Journal articles: 'Cardioprotective'

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Atwal, Kamail S., and Gary J. Grover. "Treatment of Myocardial Ischemia with ATP-Sensitive Potassium Channel (KATP) Openers." Current Pharmaceutical Design 2, no. 5 (October 1996): 585–95. http://dx.doi.org/10.2174/1381612802666221004183709.

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ATP-sensitive potassium channel (KATP) openers are potent antihypertensive agents due to their peripheral vasodilating properties. Although KATP openers have been shown to be direct cardioprotective agents, they carry a certain degree of liability for their use as cardioprotective agents. Their potent coronary and peripheral vasodilating properties can cause complications such as coronary artery steal and hypotension resulting in underperfusion of the tissue already at risk. Also, cardioprotection is not related to action potential shortening and the development of agents devoid of this activity would be desirable. Recent studies indicate that the beneficial effects of myocardial preconditioning might be mediated via opening of the KATP· Therefore, the opening of KATP might constitute an endogenous protective mechanism used by the heart under ischemic stress. Development of therapeutics to mimic this powerful protective mechanism is an attractive approach for the discovery of myocardial protecting agents. In this review, we describe the progress made towards understanding the cardioprotective properties of KATP openers including the discovery of agents that might offer a higher margin of safety for the treatment of myocardial ischemia with this class of agents. We found distinct structure-activity relationships for the cardioprotective and vasorelaxant potencies of KATP openers. Based on the structure-activity relationship studies, we were able to find cardioprotective KATP openers (BMS- 180448) which, despite being equipotent to the first generation agents (e.g., cromakalim) as cardioprotectants, had lower vasorelaxant potencies. The cardioprotecti ve effects of these selective KA TP openers in animal models of myocardial ischemia-reperfusion are also discussed in this review.

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Gupta, I., A. Goyal, NK Singh, HN Yadav, and PL Sharma. "Hemin, a heme oxygenase-1 inducer, restores the attenuated cardioprotective effect of ischemic preconditioning in isolated diabetic rat heart." Human & Experimental Toxicology 36, no. 8 (October 12, 2016): 867–75. http://dx.doi.org/10.1177/0960327116673169.

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Background: Attenuated cardioprotective effect of ischemic preconditioning (IPC) by reduced nitric oxide (NO) is a hallmark during diabetes mellitus (DM). Recently, we reported that the formation of caveolin–endothelial nitric oxide synthase (eNOS) complex decreases the release of NO, which is responsible for attenuation of IPC-induced cardioprotection in DM rat heart. Heme oxygenase-1 (HO-1) facilitates release of NO by disrupting caveolin–eNOS complex. The activity of HO-1 is decreased during DM. This study was designed to investigate the role of hemin (HO-1 inducer) in attenuated cardioprotective effect of IPC in isolated diabetic rat heart. Methods: DM was induced in male Wistar rat by single dose of streptozotocin. Cardioprotective effect was assessed in terms of myocardial infarct size and release of lactate dehydrogenase and creatine kinase in coronary effluent. The release of NO was estimated indirectly by measuring the release of nitrite in coronary effluent. Perfusion of sodium nitrite, a precursor of NO, was used as a positive control. Result: IPC-induced cardioprotection and increased release of nitrite were significantly attenuated in a diabetic rat as compared to a normal rat. Pretreatment with hemin and daidzein, a caveolin inhibitor, alone or in combination significantly restored the attenuated cardioprotection and increased the release of nitrite in diabetic rat heart. Zinc protoporphyrin, a HO-1 inhibitor, significantly abolished the observed cardioprotection and decreased the release of nitrite in hemin pretreated DM rat heart. Conclusion: Thus, it is suggested that hemin restores the attenuated cardioprotective effect in diabetic rat heart by increasing the activity of HO-1 and subsequently release of NO.

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Huh, Joon, Garrett J. Gross, Hiroshi Nagase, and Bruce T. Liang. "Protection of cardiac myocytes via δ1-opioid receptors, protein kinase C, and mitochondrial KATP channels." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 1 (January 1, 2001): H377—H383. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h377.

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The objective of the present study was to investigate the role of δ1-opioid receptors in mediating cardioprotection in isolated chick cardiac myocytes and to investigate whether protein kinase C and mitochondrial ATP-sensitive K+(KATP) channels act downstream of the δ1-opioid receptor in mediating this beneficial effect. A 5-min preexposure to the selective δ1-opioid receptor agonist (−)-TAN-67 (1 μM) resulted in less myocyte injury during the subsequent prolonged ischemia compared with untreated myocytes. 7-Benzylidenenaltrexone, a selective δ1-opioid receptor antagonist, completely blocked the cardioprotective effect of (−)-TAN-67. Naltriben methanesulfonate, a selective δ2-opioid receptor antagonist, had only a slight inhibitory effect on (−)-TAN-67-mediated cardioprotection. Nor-binaltorphimine dihydrochloride, a κ-opioid receptor antagonist, did not affect (−)-TAN-67-mediated cardioprotection. The protein kinase C inhibitor chelerythrine and the KATP channel inhibitors glibenclamide, a nonselective KATP antagonist, and 5-hydroxydecanoic acid, a mitochondrial selective KATPantagonist, reversed the cardioprotective effect of (−)-TAN-67. These results suggest that the δ1-opioid receptor is present on cardiac myocytes and mediates a potent cardioprotective effect via protein kinase C and the mitochondrial KATP channel.

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Gross, Eric R., Jason N. Peart, Anna K. Hsu, John A. Auchampach, and Garrett J. Gross. "Extending the cardioprotective window using a novel δ-opioid agonist fentanyl isothiocyanate via the PI3-kinase pathway." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (June 2005): H2744—H2749. http://dx.doi.org/10.1152/ajpheart.00918.2004.

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Selective δ-opioid agonists produce delayed cardioprotection that lasts for 24–48 h in rats; however, the maximum length of the cardioprotective window is unclear. In this study, we attempted to prolong the cardioprotective window using a unique δ-opioid agonist, fentanyl isothiocyanate (FIT), which binds irreversibly to the δ-receptor, and determined the role of the phosphatidylinositol 3-kinase (PI3K) pathway as a trigger or end effector of FIT-induced cardioprotection. Initially, male rats were administered FIT (10 μg/kg) 10 min before hearts were subjected to 30 min of ischemia and 2 h of reperfusion followed by infarct size (IS) assessment. Acute FIT administration reduced IS when given before ischemia, 5 min before reperfusion, or 10 s after reperfusion compared with control. IS reduction also occurred following a single dose of FIT at 48, 72, 96, and 120 h after administration vs. control, with the maximum effect observed at 96 h. FIT-induced IS reduction at 96 h was completely abolished when the irreversible PI3K inhibitor wortmannin (15 μg/kg) was given before FIT during the trigger phase; however, the effect was only partially abrogated when wortmannin was given 96 h later. These data suggest that FIT has a prolonged cardioprotective window greater than that of any previously described cardioprotective agent that requires PI3K primarily in the trigger phase but also partially, as a mediator or end effector.

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Schultz, Jo El J., Anna K. Hsu, Hiroshi Nagase, and Garrett J. Gross. "TAN-67, a δ1-opioid receptor agonist, reduces infarct size via activation of Gi/oproteins and KATPchannels." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 3 (March 1, 1998): H909—H914. http://dx.doi.org/10.1152/ajpheart.1998.274.3.h909.

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We have previously shown that delta (δ)-opioid receptors, most notably δ1, are involved in the cardioprotective effect of ischemic preconditioning (PC) in rats; however, the mechanism by which δ-opioid receptor-induced cardioprotection is mediated remains unknown. Therefore, we hypothesized that several of the known mediators of ischemic PC such as the ATP-sensitive potassium (KATP) channel and Gi/oproteins are involved in the cardioprotective effect produced by δ1-opioid receptor activation. To address these possibilities, anesthetized, open-chest Wistar rats were randomly assigned to five groups. Control animals were subjected to 30 min of coronary artery occlusion and 2 h of reperfusion. To demonstrate that stimulating δ1-opioid receptors produces cardioprotection, TAN-67, a new selective δ1-agonist, was infused for 15 min before the long occlusion and reperfusion periods. In addition, one group received 7-benzylidenenaltrexone (BNTX), a selective δ1-antagonist, before TAN-67. To study the involvement of KATPchannels or Gi/oproteins in δ1-opioid receptor-induced cardioprotection, glibenclamide (Glib), a KATPchannel antagonist, or pertussis toxin (PTX), an inhibitor of Gi/oproteins, was administered before TAN-67. Infarct size (IS) as a percentage of the area at risk (IS/AAR) was determined by tetrazolium stain. TAN-67 significantly reduced IS/AAR as compared with control (56 ± 2 to 27 ± 5%, n = 5, P < 0.05). The cardioprotective effect of TAN-67 was completely abolished by BNTX, Glib, and PTX (51 ± 3, 53 ± 5, and 61 ± 4%, n = 6 for each group, respectively). These results are the first to suggest that stimulating the δ1-opioid receptor elicits a cardioprotective effect that is mediated via Gi/oproteins and KATPchannels in the intact rat heart.

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Intachai, Kannaporn, Siriporn C. Chattipakorn, Nipon Chattipakorn, and Krekwit Shinlapawittayatorn. "Revisiting the Cardioprotective Effects of Acetylcholine Receptor Activation against Myocardial Ischemia/Reperfusion Injury." International Journal of Molecular Sciences 19, no. 9 (August 21, 2018): 2466. http://dx.doi.org/10.3390/ijms19092466.

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Acute myocardial infarction (AMI) is the most common cause of acute myocardial injury and its most clinically significant form. The most effective treatment for AMI is to restore an adequate coronary blood flow to the ischemic myocardium as quickly as possible. However, reperfusion of an ischemic region can induce cardiomyocyte death, a phenomenon termed “myocardial ischemia/reperfusion (I/R) injury”. Disruption of cardiac parasympathetic (vagal) activity is a common hallmark of a variety of cardiovascular diseases including AMI. Experimental studies have shown that increased vagal activity exerts cardioprotective effects against myocardial I/R injury. In addition, acetylcholine (ACh), the principle cardiac vagal neurotransmitter, has been shown to replicate the cardioprotective effects of cardiac ischemic conditioning. Moreover, studies have shown that cardiomyocytes can synthesize and secrete ACh, which gives further evidence concerning the importance of the non-neuronal cholinergic signaling cascades. This suggests that the activation of ACh receptors is involved in cardioprotection against myocardial I/R injury. There are two types of ACh receptors (AChRs), namely muscarinic and nicotinic receptors (mAChRs and nAChRs, respectively). However, the effects of AChRs activation in cardioprotection during myocardial I/R are still not fully understood. In this review, we summarize the evidence suggesting the association between AChRs activation with both electrical and pharmacological interventions and the cardioprotection during myocardial I/R, as well as outline potential mechanisms underlying these cardioprotective effects.

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Pyle, W. Glen, Yi Chen, and Polly A. Hofmann. "Cardioprotection through a PKC-dependent decrease in myofilament ATPase." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (September 2003): H1220—H1228. http://dx.doi.org/10.1152/ajpheart.00076.2003.

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Activation of myocardial κ-opioid receptor-protein kinase C (PKC) pathways may improve postischemic contractile function through a myofilament reduction in ATP utilization. To test this, we first examined the effects of PKC inhibitors on κ-opioid receptor-dependent cardioprotection. The κ-opioid receptor agonist U50,488H (U50) increased postischemic left ventricular developed pressure and reduced postischemic end-diastolic pressure compared with controls. PKC inhibitors abolished the cardioprotective effects of U50. To determine whether κ-opioid-PKC-dependent decreases in Ca2+-dependent actomyosin Mg2+-ATPase could account for cardioprotection, we subjected hearts to three separate actomyosin ATPase-lowering protocols. We observed that moderate decreases in myofibrillar ATPase were equally cardioprotective as κ-opioid receptor stimulation. Immunoblot analysis and confocal microscopy revealed a κ-opioid-induced increase in myofilament-associated PKC-ϵ, and myofibrillar Ca2+-independent PKC activity was increased after κ-opioid stimulation. This PKC-myofilament association led to an increase in troponin I and C-protein phosphorylation. Thus we propose PKC-ϵ activation and translocation to the myofilaments causes a decrease in actomyosin ATPase, which contributes to the κ-opioid receptor-dependent cardioprotective mechanism.

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Tonkovic-Capin, Marija, Garrett J. Gross, Zeljko J. Bosnjak, James S. Tweddell, Colleen M. Fitzpatrick, and John E. Baker. "Delayed cardioprotection by isoflurane: role of KATP channels." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 1 (July 1, 2002): H61—H68. http://dx.doi.org/10.1152/ajpheart.01040.2001.

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Isoflurane mimics the cardioprotective effect of acute ischemic preconditioning with an acute memory phase. We determined whether isoflurane can induce delayed cardioprotection, the involvement of ATP-sensitive potassium (KATP) channels, and cellular location of the channels. Neonatal New Zealand White rabbits at 7–10 days of age ( n = 5–16/group) were exposed to 1% isoflurane-100% oxygen for 2 h. Hearts exposed 2 h to 100% oxygen served as untreated controls. Twenty-four hours later resistance to myocardial ischemia was determined using an isolated perfused heart model. Isoflurane significantly reduced infarct size/area at risk (means ± SD) by 50% (10 ± 5%) versus untreated controls (20 ± 6%). Isoflurane increased recovery of preischemic left ventricular developed pressure by 28% (69 ± 4%) versus untreated controls (54 ± 6%). The mitochondrial KATP channel blocker 5-hydroxydecanoate (5-HD) completely (55 ± 3%) and the sarcolemmal KATPchannel blocker HMR 1098 partially (62 ± 3%) attenuated the cardioprotective effects of isoflurane. The combination of 5-HD and HMR-1098 completely abolished the cardioprotective effect of isoflurane (56 ± 5%). We conclude that both mitochondrial and sarcolemmal KATP channels contribute to isoflurane-induced delayed cardioprotection.

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Zhang, Jimmy, Sergiy M. Nadtochiy, William R. Urciuoli, and Paul S. Brookes. "The cardioprotective compound cloxyquin uncouples mitochondria and induces autophagy." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 1 (January 1, 2016): H29—H38. http://dx.doi.org/10.1152/ajpheart.00926.2014.

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Mitochondrial quality control mechanisms have been implicated in protection against cardiac ischemia-reperfusion (IR) injury. Previously, cloxyquin (5-chloroquinolin-8-ol) was identified via phenotypic screening as a cardioprotective compound. Herein, cloxyquin was identified as a mitochondrial uncoupler in both isolated heart mitochondria and adult cardiomyocytes. Additionally, cardiomyocytes isolated from transgenic mice expressing green fluorescent protein-tagged microtubule-associated protein light chain 3 showed increased autophagosome formation with cloxyquin treatment. The autophagy inhibitor chloroquine abolished cloxyquin-induced cardioprotection in both cellular and perfused heart (Langendorff) models of IR injury. Finally, in an in vivo murine left anterior descending coronary artery occlusion model of IR injury, cloxyquin significantly reduced infarct size from 31.4 ± 3.4% to 16.1 ± 2.2%. In conclusion, the cardioprotective compound cloxyquin simultaneously uncoupled mitochondria and induced autophagy. Importantly, autophagy appears to be required for cloxyquin-induced cardioprotection.

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Liu, Shu Q., Brandon J. Tefft, Derek T. Roberts, Li-Qun Zhang, Yupeng Ren, Yan Chun Li, Yong Huang, Di Zhang, Harry R. Phillips, and Yu H. Wu. "Cardioprotective proteins upregulated in the liver in response to experimental myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 12 (December 15, 2012): H1446—H1458. http://dx.doi.org/10.1152/ajpheart.00362.2012.

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Myocardial ischemia (MI) activates innate cardioprotective mechanisms, enhancing cardiomyocyte tolerance to ischemia. Here, we report a MI-activated liver-dependent mechanism for myocardial protection. In response to MI in the mouse, hepatocytes exhibited 6- to 19-fold upregulation of genes encoding secretory proteins, including α-1-acid glycoprotein (AGP)2, bone morphogenetic protein-binding endothelial regulator (BMPER), chemokine (C-X-C motif) ligand 13, fibroblast growth factor (FGF)21, neuregulin (NRG)4, proteoglycan 4, and trefoil factor (TFF)3. Five of these proteins, including AGP2, BMPER, FGF21, NRG4, and TFF3, were identified as cardioprotective proteins since administration of each protein significantly reduced the fraction of myocardial infarcts (37 ± 9%, 34 ± 7%, 32 ± 8%, 39 ± 6%, and 31 ± 7%, respectively, vs. 48 ± 7% for PBS at 24 h post-MI). The serum level of the five proteins elevated significantly in association with protein upregulation in hepatocytes post-MI. Suppression of a cardioprotective protein by small interfering (si)RNA-mediated gene silencing resulted in a significant increase in the fraction of myocardial infarcts, and suppression of all five cardioprotective proteins with siRNAs further intensified myocardial infarction. While administration of a single cardioprotective protein mitigated myocardial infarction, administration of all five proteins furthered the beneficial effect, reducing myocardial infarct fractions from PBS control values from 46 ± 6% (5 days), 41 ± 5% (10 days), and 34 ± 4% (30 days) to 35 ± 5%, 28 ± 5%, and 24 ± 4%, respectively. These observations suggest that the liver contributes to cardioprotection in MI by upregulating and releasing protective secretory proteins. These proteins may be used for the development of cardioprotective agents.

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Campbell, Duncan J. "Therapeutic modulation of tissue kallikrein expression." Biological Chemistry 397, no. 12 (December 1, 2016): 1293–97. http://dx.doi.org/10.1515/hsz-2016-0167.

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Abstract The kallikrein kinin system has cardioprotective actions and mediates in part the cardioprotection produced by angiotensin converting enzyme inhibitors and angiotensin type 1 receptor blockers. Additional approaches to exploit the cardioprotective effects of the kallikrein kinin system include the administration of tissue kallikrein and kinin receptor agonists. The renin inhibitor aliskiren was recently shown to increase cardiac tissue kallikrein expression and bradykinin levels, and to reduce myocardial ischemia-reperfusion injury by bradykinin B2 receptor- and angiotensin AT2 receptor-mediated mechanisms. Thus, aliskiren represents a prototype drug for the modulation of tissue kallikrein expression for therapeutic benefit.

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Sevrukevitch, V. V., and F. I. Vismont. "CARDIOPROTECTIVE EFFICIENCY OF THE COMBINED APPLICATION OF REMOTE ISCHEMIC PRE- AND POST-CONDITIONING IN RATS IN CASE OF MIOCARDIAL ISCHEMIA/REPERFUSION." Emergency Cardiology and Cardiovascular Risks 4, no. 2 (2020): 1045–47. http://dx.doi.org/10.51922/2616-633x.2020.4.2.1045.

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The cardioprotective efficacy of the combined use of remote ischemic preconditioning (RIPreC) and remote ischaemic postconditioning (RIPostC) in experimental myocardial ischemia/reperfusion was studied in rats. Experimental myocardial ischemia/reperfusion was reproduced by a 30-minute occlusion of the left coronary artery followed by a period of 120-minute reperfusion. Remote ischemic conditioning was reproduced by short-term occlusion of both femoral arteries followed by reperfusion of the extremities beginning at the following time points: RIPreC– 25 minutes before the end of the myocardial ischemia period, RIPostC - 10 minutes after the end of the myocardial ischemia period, RIPreC + RIPostC– 25 minutes before the start and 10 minutes after the end of myocardial ischemia. It was shown that the combined use of RIPreC and RIPostC had a comparable cardioprotective effect in comparison with each of these methods taken separately. Possible reasons explaining the lack of potentiation of the cardioprotective effect of the combined use of RIPreC with RIPostC can presumably be attributed to: 1) achieving maximum cardioprotection, i.e. the impossibility to further reduce the area of myocardial ischemia, 2) the effect on similar intracellular cardioprotective mechanisms in different conditioning modes.

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Maddaford, Thane G., and Grant N. Pierce. "Myocardial dysfunction is associated with activation of Na+/H+exchange immediately during reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 5 (November 1, 1997): H2232—H2239. http://dx.doi.org/10.1152/ajpheart.1997.273.5.h2232.

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Amiloride analogs block Na+/H+exchange and thereby protect the heart from myocardial ischemia-reperfusion injury. It is unclear whether drugs must be present before ischemia to be cardioprotective. After 60 min of global ischemia in the coronary-perfused right ventricular wall (RVW), as little as 1 min of exposure to dimethyl amiloride (DMA) immediately at the time of reperfusion protected the RVW. Delaying the drug attenuated the cardioprotection. If DMA was introduced in an ischemic solution near the end of ischemia, the cardioprotective effects were augmented. If the drug was washed out of the RVW vascular space before ischemia, cardioprotection was not observed. In contrast, in whole hearts, preischemic perfusion of the drug was necessary for cardioprotection and the cardioprotection remained even if the drug was washed out before ischemia. We conclude that Na+/H+exchange is active and contributes to contractile dysfunction during the first seconds of reperfusion. This is difficult to detect in the perfused whole heart, and the washout data suggest that this may be due to a limitation in drug delivery across the vascular wall. The data also suggest that the exchanger is not as active during ischemia itself as it is during reperfusion.

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Dickson, Eric W., Christopher P. Hogrefe, Paula S. Ludwig, Laynez W. Ackermann, Lynn L. Stoll, and Gerene M. Denning. "Exercise enhances myocardial ischemic tolerance via an opioid receptor-dependent mechanism." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 1 (January 2008): H402—H408. http://dx.doi.org/10.1152/ajpheart.00280.2007.

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Exercise increases serum opioid levels and improves cardiovascular health. Here we tested the hypothesis that opioids contribute to the acute cardioprotective effects of exercise using a rat model of exercise-induced cardioprotection. For the standard protocol, rats were randomized to 4 days of treadmill training and 1 day of vigorous exercise ( day 5), or to a sham exercise control group. On day 6, animals were killed, and global myocardial ischemic tolerance was assessed on a modified Langendorff apparatus. Twenty minutes of ischemia followed by 3 h of reperfusion resulted in a mean infarct size of 42 ± 4% in hearts from sham exercise controls and 21 ± 3% ( P < 0.001) in the exercised group. The cardioprotective effects of exercise were gone by 5 days after the final exercise period. To determine the role of opioid receptors in exercise-induced cardioprotection, rats were exercised according to the standard protocol; however, just before exercise on days 4 and 5, rats were injected subcutaneously with 10 mg/kg of the opioid receptor antagonist naltrexone. Similar injections were performed in the sham exercise control group. Naltrexone had no significant effect on baseline myocardial ischemic tolerance in controls (infarct size 43 ± 4%). In contrast, naltrexone treatment completely blocked the cardioprotective effect of exercise (infarct size 40 ± 5%). Exercise was also associated with an early increase in myocardial mRNA levels for several opioid system genes and with sustained changes in a number of genes that regulate inflammation and apoptosis. These findings demonstrate that the acute cardioprotective effects of exercise are mediated, at least in part, through opioid receptor-dependent mechanisms that may include changes in gene expression.

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Li, Jianqiang, Danghui Sun, and Yue Li. "Novel Findings and Therapeutic Targets on Cardioprotection of Ischemia/ Reperfusion Injury in STEMI." Current Pharmaceutical Design 25, no. 35 (December 11, 2019): 3726–39. http://dx.doi.org/10.2174/1381612825666191105103417.

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Acute ST-segment elevation myocardial infarction (STEMI) remains a leading cause of morbidity and mortality around the world. A large number of STEMI patients after the infarction gradually develop heart failure due to the infarcted myocardium. Timely reperfusion is essential to salvage ischemic myocardium from the infarction, but the restoration of coronary blood flow in the infarct-related artery itself induces myocardial injury and cardiomyocyte death, known as ischemia/reperfusion injury (IRI). The factors contributing to IRI in STEMI are complex, and microvascular obstruction, inflammation, release of reactive oxygen species, myocardial stunning, and activation of myocardial cell death are involved. Therefore, additional cardioprotection is required to prevent the heart from IRI. Although many mechanical conditioning procedures and pharmacological agents have been identified as effective cardioprotective approaches in animal studies, their translation into the clinical practice has been relatively disappointing due to a variety of reasons. With new emerging data on cardioprotection in STEMI over the past few years, it is mandatory to reevaluate the effectiveness of “old” cardioprotective interventions and highlight the novel therapeutic targets and new treatment strategies of cardioprotection.

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Caricati-Neto, Afonso, Paolo Ruggero Errante, and Francisco Sandro Menezes-Rodrigues. "Recent Advances in Pharmacological and Non-Pharmacological Strategies of Cardioprotection." International Journal of Molecular Sciences 20, no. 16 (August 16, 2019): 4002. http://dx.doi.org/10.3390/ijms20164002.

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Ischemic heart diseases (IHD) are the leading cause of death worldwide. Although the principal form of treatment of IHD is myocardial reperfusion, the recovery of coronary blood flow after ischemia can cause severe and fatal cardiac dysfunctions, mainly due to the abrupt entry of oxygen and ionic deregulation in cardiac cells. The ability of these cells to protect themselves against injury including ischemia and reperfusion (I/R), has been termed “cardioprotection”. This protective response can be stimulated by pharmacological agents (adenosine, catecholamines and others) and non-pharmacological procedures (conditioning, hypoxia and others). Several intracellular signaling pathways mediated by chemical messengers (enzymes, protein kinases, transcription factors and others) and cytoplasmic organelles (mitochondria, sarcoplasmic reticulum, nucleus and sarcolemma) are involved in cardioprotective responses. Therefore, advancement in understanding the cellular and molecular mechanisms involved in the cardioprotective response can lead to the development of new pharmacological and non-pharmacological strategies for cardioprotection, thus contributing to increasing the efficacy of IHD treatment. In this work, we analyze the recent advances in pharmacological and non-pharmacological strategies of cardioprotection.

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Makkos, András, Bence Ágg, Zoltán V. Varga, Zoltán Giricz, Mariann Gyöngyösi, Dominika Lukovic, Rainer Schulz, Monika Barteková, Anikó Görbe, and Péter Ferdinandy. "Molecular Network Approach Reveals Rictor as a Central Target of Cardiac ProtectomiRs." International Journal of Molecular Sciences 22, no. 17 (September 2, 2021): 9539. http://dx.doi.org/10.3390/ijms22179539.

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Cardioprotective medications are still unmet clinical needs. We have previously identified several cardioprotective microRNAs (termed ProtectomiRs), the mRNA targets of which may reveal new drug targets for cardioprotection. Here we aimed to identify key molecular targets of ProtectomiRs and confirm their association with cardioprotection in a translational pig model of acute myocardial infarction (AMI). By using a network theoretical approach, we identified 882 potential target genes of 18 previously identified protectomiRs. The Rictor gene was the most central and it was ranked first in the protectomiR-target mRNA molecular network with the highest node degree of 5. Therefore, Rictor and its targeting microRNAs were further validated in heart samples obtained from a translational pig model of AMI and cardioprotection induced by pre- or postconditioning. Three out of five Rictor-targeting pig homologue of rat ProtectomiRs showed significant upregulation in postconditioned but not in preconditioned pig hearts. Rictor was downregulated at the mRNA and protein level in ischemic postconditioning but not in ischemic preconditioning. This is the first demonstration that Rictor is the central molecular target of ProtectomiRs and that decreased Rictor expression may regulate ischemic postconditioning-, but not preconditioning-induced acute cardioprotection. We conclude that Rictor is a potential novel drug target for acute cardioprotection.

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Dominguez-Rodriguez, Alberto, Pedro Abreu-Gonzalez, and Yundai Chen. "Cardioprotection and effects of melatonin administration on cardiac ischemia reperfusion: Insight from clinical studies." Melatonin Research 2, no. 2 (June 12, 2019): 100–105. http://dx.doi.org/10.32794/mr11250024.

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Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality. Many treatments have been identified that confer robust cardioprotection in experimental animal models of acute ischemia and reperfusion injury. However, translation of these cardioprotective therapies into the clinical setting of AMI for patient benefit has been disappointing. Many cardioprotective strategies act through common end-effectors and may be suboptimal in patients with comorbidities. Melatonin is a pleiotropic molecule with several functions. Its potential to protect the heart against ischemia/reperfusion damage has attracted much attention, particularly in view of its possible clinical applications. In this brief overview, we discuss the possible clinical application of melatonin in human.

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Karwi, Yahya G., Inam S. Arif, and Muthanna I. Al-Ezzi. "The potential protective effect of metformin on selective cardiac biomarkers in diabetic male rats." Al Mustansiriyah Journal of Pharmaceutical Sciences 17, no. 1 (March 13, 2018): 7. http://dx.doi.org/10.32947/ajps.v17i1.65.

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Metformin, a biguanide, first line antidiabetic agent, undergoes extensive debate to explain its possible cardioprotective effect. This study represents an attempt to help clarifying this cardioprotective effect. 24rats divided into three diabetic group (8 rats for each) (diabetes induced by Streptozocin 60 mg/kgi.p.). Diabetic groups treated with (saline, 75 mg/kg metformin and 150 mg/kg metformin, i.p.) for 6 weeks, then cardiac stress was induced by isoproterenol (ISO) (150 mg/kg i.p.) for two successive days. Selective biomarkers were assessed; brain natriuretic peptide (BNP), matrix metalloproteinase - 1 (MMP-1) and histopathology examination. The results of this study showed that metformin produce a dose dependent cardioprotection effect in diabetic rats.

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Wang, Yves T., Yunki Lim, Matthew N. McCall, Kai-Ting Huang, Cole M. Haynes, Keith Nehrke, and Paul S. Brookes. "Cardioprotection by the mitochondrial unfolded protein response requires ATF5." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 2 (August 1, 2019): H472—H478. http://dx.doi.org/10.1152/ajpheart.00244.2019.

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The mitochondrial unfolded protein response (UPRmt) is a cytoprotective signaling pathway triggered by mitochondrial dysfunction. UPRmt activation upregulates chaperones, proteases, antioxidants, and glycolysis at the gene level to restore proteostasis and cell energetics. Activating transcription factor 5 (ATF5) is a proposed mediator of the mammalian UPRmt. Herein, we hypothesized pharmacological UPRmt activation may protect against cardiac ischemia-reperfusion (I/R) injury in an ATF5-dependent manner. Accordingly, in vivo administration of the UPRmt inducers oligomycin or doxycycline 6 h before ex vivo I/R injury (perfused heart) was cardioprotective in wild-type but not global Atf5−/− mice. Acute ex vivo UPRmt activation was not cardioprotective, and loss of ATF5 did not impact baseline I/R injury without UPRmt induction. In vivo UPRmt induction significantly upregulated many known UPRmt-linked genes (cardiac quantitative PCR and Western blot analysis), and RNA-Seq revealed an UPRmt-induced ATF5-dependent gene set, which may contribute to cardioprotection. This is the first in vivo proof of a role for ATF5 in the mammalian UPRmt and the first demonstration that UPRmt is a cardioprotective drug target. NEW & NOTEWORTHY Cardioprotection can be induced by drugs that activate the mitochondrial unfolded protein response (UPRmt). UPRmt protection is dependent on activating transcription factor 5 (ATF5). This is the first in vivo evidence for a role of ATF5 in the mammalian UPRmt.

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AL-YAHYA, ABDULRAHMAN A. I., MOHAMMED ASAD, ABDULMONIEM SADABY, and KHALID ELFAKKI IBRAHIM. "Short Communication: Augmentation of cardioprotective effect of captopril by Costus speciosus against isoproterenol induced myocardial toxicity in rats." Nusantara Bioscience 9, no. 3 (August 2, 2017): 295–99. http://dx.doi.org/10.13057/nusbiosci/n090309.

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Al-Yahya AAI, Asad M, Sadaby A, Ibrahim KE. 2017. Short Communication: Augmentation of cardioprotective effect of captopril by Costus speciosus against isoproterenol induced myocardial toxicity in rats. Nusantara Bioscience 9: 295-299. This study determined the pharmacodynamic interaction of captopril, a known cardioprotective effect with methanolic extract of Costus speciosus rhizomes (Costaceae) that is known for its powerful antioxidant action during isoproterenol induced cardiac toxicity in rats. A methanolic extract of the rhizomes was prepared by maceration. Rats were administered the methanolic extract at two different doses of 200 mg/k or 400 mg/kg orally and captopril was administered orally at a dose of 30 mg/kg. All the drugs alone or in combination were once daily for two weeks. At the end of treatment period, two doses of isoproterenol (150 mg/kg, s.c) were administered to rats at 24 hr interval. Blood was withdrawn to estimate creatinine kinase-MB (CK-MB) activities. The heart tissue was subjected to histological examinations to determine the extent of damage. Isoproterenol induced severe damage to the myocardium that was indicated through an elevation in serum CK-MB activity and the same was confirmed by histological examinations. Costus speciosus at both the tested doses attenuated the damage produced by isoproterenol. Both the doses caused a decrease in the biomarker activity as well as reduced the myocardial damage as observed in histological examination. A similar effect was observed with captopril. The co-administration of captopril with either dose of Costus speciosus demonstrated excellent cardioprotection suggesting that combination of this herb with captopril augments its cardioprotective action. It was concluded that Costus speciosus shows dose-dependent cardioprotection and augments the cardioprotective effect of captopril during isoproterenol induced cardiotoxicity in rats.

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Randhawa, Puneet Kaur, and Amteshwar Singh Jaggi. "Opioids in Remote Ischemic Preconditioning-Induced Cardioprotection." Journal of Cardiovascular Pharmacology and Therapeutics 22, no. 2 (July 28, 2016): 112–21. http://dx.doi.org/10.1177/1074248416660621.

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Remote ischemic preconditioning (RIPC) is an intriguing process whereby transient regional ischemia and reperfusion episodes to remote tissues including skeletal, renal, mesenteric provide protection to the heart against sustained ischemia–reperfusion-induced injury. Clinically, this technique has been used in patients undergoing various surgical interventions including coronary artery bypass graft surgery, abdominal aortic aneurysm repair, percutaneous coronary intervention, and heart valve surgery. The endogenous opioid system is extensively expressed in the brain to modulate pain sensation. Besides the role of opioids in relieving pain, numerous researchers have found their critical involvement in evoking cardioprotective effects. Endogenous opioids including endorphins, enkephalins, and dynorphins are released during RIPC and are critically involved in mediating RIPC-induced cardioprotective effects. It has been suggested that during RIPC, the endogenous opioids may be released into the systemic circulation and may travel via bloodstream that act on the myocardial opioid receptors to induce cardioprotection. The present review describes the potential role of opioids in mediating RIPC-induced cardioprotection.

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Johnson, Norman A., and Stephanie de Bono. "Cardioprotective cysteine." Trends in Biochemical Sciences 27, no. 7 (July 2002): 337–38. http://dx.doi.org/10.1016/s0968-0004(02)02153-9.

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Abdellatif, Maha. "Cardioprotective MicroRNAs." Pediatric Cardiology 32, no. 3 (January 19, 2011): 311–16. http://dx.doi.org/10.1007/s00246-010-9882-7.

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Zuurbier, Coert J., Otto Eerbeek, and Alfred J. Meijer. "Ischemic preconditioning, insulin, and morphine all cause hexokinase redistribution." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H496—H499. http://dx.doi.org/10.1152/ajpheart.01182.2004.

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Association of hexokinase (HK) with mitochondria preserves mitochondrial integrity and is an important mechanism by which cancer cells are protected against hypoxic conditions. Maintenance of mitochondrial integrity also figures prominently as a major characteristic of many cardioprotective manipulations. In this study, we provide evidence that cardioprotective interventions may promote HK redistribution from the cytosol to the mitochondria in the heart. Isolated Langendorff-perfused rat hearts ( n = 6/group) were subjected to normoxic perfusion (control, Con), three 5-min ischemia-reperfusion periods (ischemic preconditioning, IPC), 1 U/l insulin (Ins), or 1 μM morphine (Mor). Hearts were immediately homogenized and centrifuged to obtain whole cell, cytosolic, and mitochondrial fractions. HK, lactate dehydrogenase (LDH), and citrate synthase (CS) enzyme activities were determined. No change in LDH or CS present in the cytosol fraction relative to whole cell activity was observed with any of the cardioprotective interventions. By contrast, HK present in the cytosol fraction relative to whole cell activity decreased significantly ( P < 0.05) with all cardioprotective interventions, from 0.58 ± 0.03 (Con) to 0.46 ± 0.04 (IPC), 0.41 ± 0.01 (Ins), and 0.45 ± 0.02 (Mor). In addition, HK relative to CS activity in the mitochondrial fraction increased significantly with cardioprotection, from 0.15 ± 0.001 (Con) to 0.21 ± 0.002 (IPC), 0.18 ± 0.003 (Ins), and 0.21 ± 0.005 (Mor). Our novel data suggest that well-known cardioprotective interventions share a common end-effector mechanism of cytosolic HK translocation. Association of HK with mitochondria may promote inhibition of the mitochondrial permeability transition pore and thereby reduce cell death and apoptosis.

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Chennuru, Anusha, and Mohamed T. S. Saleem. "Antioxidant, Lipid Lowering, and Membrane Stabilization Effect of Sesamol against Doxorubicin-Induced Cardiomyopathy in Experimental Rats." BioMed Research International 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/934239.

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The present study was designed to evaluate the cardioprotective effect of sesamol against doxorubicin-induced cardiomyopathy in rats. In this study, the cardioprotective effect of sesamol against doxorubicin induced cardiomyopathy in experimental rats was evaluated at the dosage of 50 mg/kg bw. Doxorubicin was administered to rats at a total cumulative dose of 15 mg/kg through intraperitoneal route for 2 weeks in six-divided dose on 8th, 10th, 14th, 16th, 18th, and 21st day. After the last dose administration, the endogenous antioxidants and lipid peroxidation were estimated in heart tissue homogenate. Cardiac biomarkers such as troponin T, LDH, CK, and AST and lipid profiles such as cholesterol, triglycerides, HDL, LDL, and VLDL were estimated in serum. Sesamol has cardioprotective activity through normalization of doxorubicin-induced-altered biochemical parameters. Biochemical study was further supported by histopathological study, which shows that sesamol offered myocardial protection from necrotic damage. From these findings, it has been concluded that the sesamol has significant cardioprotection against doxorubicin induced cardiomyopathy via amelioration of oxidative stress, lipid lowering, and membrane stabilization effect.

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Shah, Syed Muhammad Ali, Muhammad Akram, Muhammad Riaz, Naveed Munir, and Ghulam Rasool. "Cardioprotective Potential of Plant-Derived Molecules: A Scientific and Medicinal Approach." Dose-Response 17, no. 2 (April 1, 2019): 155932581985224. http://dx.doi.org/10.1177/1559325819852243.

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Since the beginning of human civilization, plants have been used in alleviating the human distress and it was recorded for about thousands of years ago that the plants are being used for medicinal purposes. Natural bioactive compounds called phytochemicals are obtained from medicinal plants, vegetables, and fruits, which functions to combat against various ailments. There is dire need to explore the plant biodiversity for its medicinal and pharmacological potentials. Different databases such as Google scholar, Medline, PubMed, and the Directory of Open Access Journals were searched to find the articles describing the cardioprotective function of medicinal plants. Various substances from a variety of plant species are used for the treatment of cardiovascular abnormalities. The cardioprotective plants contain a variety of bioactive compounds, including diosgenin, isoflavones, sulforaphane, carotinized, catechin, and quercetin, have been proved to enhance cardioprotection, hence reducing the risk of cardiac abnormalities. The present review article provides the data on the use of medicinal plants particularly against cardiac diseases and to explore the molecules/phytoconstituents as plant secondary metabolites for their cardioprotective potential.

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Csonka, Csaba, Krisztina Kupai, Péter Bencsik, Anikó Görbe, János Pálóczi, Ágnes Zvara, László G. Puskás, Tamás Csont, and Péter Ferdinandy. "Cholesterol-enriched diet inhibits cardioprotection by ATP-sensitive K+ channel activators cromakalim and diazoxide." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 3 (February 1, 2014): H405—H413. http://dx.doi.org/10.1152/ajpheart.00257.2013.

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It has been previously shown that hyperlipidemia interferes with cardioprotective mechanisms. Here, we investigated the interaction of hyperlipidemia with cardioprotection induced by pharmacological activators of ATP-sensitive K+ (KATP) channels. Hearts isolated from rats fed a 2% cholesterol-enriched diet or normal diet for 8 wk were subjected to 30 min of global ischemia and 120 min of reperfusion in the presence or absence of KATP modulators. In normal diet-fed rats, either the nonselective KATP activator cromakalim at 10−5 M or the selective mitochondrial (mito)KATP opener diazoxide at 3 × 10−5 M significantly decreased infarct size compared with vehicle-treated control rats. Their cardioprotective effect was abolished by coadministration of the nonselective KATP blocker glibenclamide or the selective mitoKATP blocker 5-hydroxydecanoate, respectively. However, in cholesterol-fed rats, the cardioprotective effect of cromakalim or diazoxide was not observed. Therefore, we further investigated how cholesterol-enriched diet influences cardiac KATP channels. Cardiac expression of a KATP subunit gene (Kir6.1) was significantly downregulated in cholesterol-fed rats; however, protein levels of Kir6.1 and Kir6.2 were not changed. The cholesterol diet significantly decreased cardiac ATP, increased lactate content, and enhanced myocardial oxidative stress, as shown by increased cardiac superoxide and dityrosine formation. This is the first demonstration that cardioprotection by KATP channel activators is impaired in cholesterol-enriched diet-induced hyperlipidemia. The background mechanism may include hyperlipidemia-induced attenuation of mitoKATP function by altered energy metabolism and increased oxidative stress in the heart.

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Haybar, Habib, Saeid Shahrabi, Zeinab Deris Zayeri, and SeyedmohammadSadegh Pezeshki. "Strategies to increase cardioprotection through cardioprotective chemokines in chemotherapy-induced cardiotoxicity." International Journal of Cardiology 269 (October 2018): 276–82. http://dx.doi.org/10.1016/j.ijcard.2018.07.087.

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Li, Qiang, Ping Wang, Keqiang Ye, and Hua Cai. "Central role of SIAH inhibition in DCC-dependent cardioprotection provoked by netrin-1/NO." Proceedings of the National Academy of Sciences 112, no. 3 (January 5, 2015): 899–904. http://dx.doi.org/10.1073/pnas.1420695112.

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Deleted in colorectal cancer (DCC), a large transmembrane receptor of netrin-1, is critical for mediating netrin-1’s cardioprotective function. In the present study we investigated novel mechanisms underlying netrin-1–induced, rapid, and feed-forward up-regulation of DCC, which is believed to sustain nitric oxide (NO) production to potentiate cardioprotection. Intriguingly, NO markedly reduced expression of the E3 ubiquitin ligase seven in absentia homolog (SIAH) that is specific for regulation of protesome-dependent DCC degradation, resulting in accumulation of DCC. The two SIAH isoforms compensate for each other when one is repressed; inhibition of both SIAH1 and SIAH2 using combined siRNAs significantly reduced infarct size while improving cardiac function after ischemia/reperfusion injury of the heart. This effect was absent in DCC-deficient mice. Moreover, in vivo RNAi inhibition of SIAH1/2 further augmented netrin-1’s cardioprotective function. In summary, these data identify a novel therapeutic target of SIAH in facilitating NO/netrin-1–dependent cardioprotection, using the DCC receptor. Combination of netrin-1 and SIAH RNAi may prove to be a substantially effective therapy for myocardial infarction.

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Nadtochiy, Sergiy M., Hongwei Yao, Michael W. McBurney, Wei Gu, Leonard Guarente, Irfan Rahman, and Paul S. Brookes. "SIRT1-mediated acute cardioprotection." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (October 2011): H1506—H1512. http://dx.doi.org/10.1152/ajpheart.00587.2011.

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Overexpression studies have revealed a role for silent information regulator of transcription 1 (SIRT1) lysine deacetylase in cardioprotection against ischemia-reperfusion injury via long-term transcriptional effects. However, short-term SIRT1-mediated lysine deacetylation, within the context of acute cardioprotection, is poorly understood. In this study, the role of SIRT1 in the acute cardioprotective paradigm of first window ischemic preconditioning (IPC) was studied using SIRT1-deficient (SIRT1+/−) and SIRT1-overexpressing (SIRT1+++) mice. In wild-type hearts, cytosolic lysine deacetylation was observed during IPC, and overacetylation was observed upon pharmacological SIRT1 inhibition. Consistent with a role for SIRT1 in IPC, SIRT1+/− hearts could not be preconditioned and exhibited increased cytosolic lysine acetylation. Furthermore, SIRT1+++ hearts were endogenously protected against ischemia-reperfusion injury and exhibited decreased cytosolic acetylation. Both of these effects in SIRT1+++ mice were reversed by pharmacological SIRT1 inhibition on an acute timescale. Several downstream targets of SIRT1 were examined, with data suggesting possible roles for endothelial nitric oxide synthase phosphorylation, NF-κB, and stimulation of autophagy. In conclusion, these data suggest that SIRT1, acting on nontranscriptional targets, is required for cardioprotection by acute IPC and that SIRT1-dependent lysine deacetylation occurs during IPC and may play a role in cardioprotective signaling.

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Sun, Hai-Jing, Yan Lu, Hao-Wei Wang, Hao Zhang, Shuang-Ran Wang, Wen-Yun Xu, Hai-Long Fu, Xue-Ya Yao, Feng Yang, and Hong-Bin Yuan. "Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–18. http://dx.doi.org/10.1155/2017/2186383.

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Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study investigated the roles of endocannabinoid signaling in propofol cardioprotection in an in vivo model of myocardial ischemia/reperfusion (I/R) injury and in in vitro primary cardiomyocyte hypoxia/reoxygenation (H/R) injury. The results showed that propofol conditioning increased both serum and cell culture media concentrations of endocannabinoids including anandamide (AEA) and 2-arachidonoylglycerol (2-AG) detected by LC-MS/MS. The reductions of myocardial infarct size in vivo and cardiomyocyte apoptosis and death in vitro were accompanied with attenuations of oxidative injuries manifested as decreased reactive oxygen species (ROS), malonaldehyde (MDA), and MPO (myeloperoxidase) and increased superoxide dismutase (SOD) production. These effects were mimicked by either URB597, a selective endocannabinoids degradation inhibitor, or VDM11, a selective endocannabinoids reuptake inhibitor. In vivo study further validated that the cardioprotective and antioxidative effects of propofol were reversed by selective CB2 receptor antagonist AM630 but not CB1 receptor antagonist AM251. We concluded that enhancing endogenous endocannabinoid release and subsequent activation of CB2 receptor signaling represent a major mechanism whereby propofol conditioning confers antioxidative and cardioprotective effects against myocardial I/R injury.

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Calvert, John W., and David J. Lefer. "Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection." Physiology 28, no. 4 (July 2013): 216–24. http://dx.doi.org/10.1152/physiol.00011.2013.

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Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.

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Fathima, Syeda Nishat, and Vasudeva Murthy S. "CURRENT PHARMACOLOGICAL STATUS OF CARDIOPROTECTIVE PLANTS AGAINST ISOPROTERENOL INDUCED MYOCARDIAL INFARCTION." Asian Journal of Pharmaceutical and Clinical Research 11, no. 4 (April 1, 2018): 17. http://dx.doi.org/10.22159/ajpcr.2018.v11i4.24158.

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Objective: Cardiovascular diseases are the major cause of morbidity and mortality in the modern era. Myocardial infarction is a condition where there is a significant decrease or block in the blood (oxygen) supply to the part of heart, leading to degeneration of a portion of the myocardium which triggers a cascade of cellular, inflammatory and biochemical events, leading eventually to the irreversible death (necrosis) of heart muscle cells. Various therapeutic interventions, including lifestyle modification, pharmacological treatment options, and surgical techniques are available. The present review focus on the plants that have been evaluated for cardioprotective activity against isoproterenol-induced myocardial infarction.Method: The current status of Cardioprotective plants was obtained from a literature search of electronic databases such as Google Scholar, Pubmed and Scopus up to 2017 for publications on medicinal plants used against isoproterenol-induced myocardial infarction. Isoproterenol, Isoprenaline, myocardial infarction, cardioprotective were used as keywords for the searching.Result: A total of 117 different plant parts and their extracts have till now been published to possess cardioprotection against isoproterenol-induced myocardial infarction. Isoproterenol a beta-adrenergic receptors agonist causes severe stress in myocardium resulting in the infarct-like lesion and produced cardiotoxic effects by elevating the levels of cardiac biomarkers and causing changes in ECG. Plant-based medicines with their antioxidant, antiapoptotic, antihyperlipidemic, platelet antiaggregatory, anti-lipid peroxidation property provide substantial evidence for the management of Ischemia.Conclusion: This review, therefore, provides a useful resource to enable a thorough assessment of the profile of plants that have cardioprotective activity against isoproterenol-induced myocardial infarction.

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Rowland, R. T., X. Meng, J. C. Cleveland, D. R. Meldrum, A. H. Harken, and J. M. Brown. "LPS-induced delayed myocardial adaptation enhances acute preconditioning to optimize postischemic cardiac function." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (June 1, 1997): H2708—H2715. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2708.

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Myocardial tolerance to ischemia and reperfusion (I/R) injury can be achieved by either acute or delayed cardioprotective mechanisms. Ischemic preconditioning has been demonstrated to be a powerful acute cardioprotective stimulus. We have reported that lipopolysaccharide (LPS) pretreatment induces delayed myocardial adaptation to I/R injury. To optimize myocardial protection, we examined the ability of delayed myocardial adaptation to enhance acute ischemic preconditioning in the isolated working rat heart. Male Sprague-Dawley rats were divided into control, acute [transient ischemia (TI); 5-min global ischemia, 37 degrees C], delayed (LPS; 500 micrograms/kg i.p.), or combined (LPS + TI) cardioprotective groups. Delayed cardioprotection involved LPS injection 72 h before heart isolation. All hearts were subjected to 20-min global ischemia (37 degrees C) and 30-min reperfusion. Coronary effluent collected during reperfusion was assayed for creatine kinase (CK) activity. Both TI and LPS treatment improved postischemic aortic flow recovery (29 +/- 4.5 and 44 +/- 4.0%, respectively; P < 0.05, LPS vs. TI) compared with control hearts (11 +/- 2.2%; P < 0.05, TI or LPS vs. control). When TI was applied to LPS-treated hearts (LPS + TI), aortic flow recovery was further enhanced (57 +/- 3.8%; P < 0.05 vs. TI or LPS alone). CK release during 20 and 30 min of reperfusion was decreased in all treated hearts compared with control hearts (P < 0.05). These results indicate that delayed myocardial adaptation and acute ischemic preconditioning independently activate protective mechanisms against ischemia. Enhanced protection occurs when induced delayed mechanisms are combined with acute cardioprotective stimuli, which optimize postischemic myocardial function and reduce myocellular necrosis.

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Chung, Youn Wook, Claudia Lagranha, Yong Chen, Junhui Sun, Guang Tong, Steven C. Hockman, Faiyaz Ahmad, et al. "Targeted disruption of PDE3B, but not PDE3A, protects murine heart from ischemia/reperfusion injury." Proceedings of the National Academy of Sciences 112, no. 17 (April 15, 2015): E2253—E2262. http://dx.doi.org/10.1073/pnas.1416230112.

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Although inhibition of cyclic nucleotide phosphodiesterase type 3 (PDE3) has been reported to protect rodent heart against ischemia/reperfusion (I/R) injury, neither the specific PDE3 isoform involved nor the underlying mechanisms have been identified. Targeted disruption of PDE3 subfamily B (PDE3B), but not of PDE3 subfamily A (PDE3A), protected mouse heart from I/R injury in vivo and in vitro, with reduced infarct size and improved cardiac function. The cardioprotective effect in PDE3B−/− heart was reversed by blocking cAMP-dependent PKA and by paxilline, an inhibitor of mitochondrial calcium-activated K channels, the opening of which is potentiated by cAMP/PKA signaling. Compared with WT mitochondria, PDE3B−/− mitochondria were enriched in antiapoptotic Bcl-2, produced less reactive oxygen species, and more frequently contacted transverse tubules where PDE3B was localized with caveolin-3. Moreover, a PDE3B−/− mitochondrial fraction containing connexin-43 and caveolin-3 was more resistant to Ca2+-induced opening of the mitochondrial permeability transition pore. Proteomics analyses indicated that PDE3B−/− heart mitochondria fractions were enriched in buoyant ischemia-induced caveolin-3–enriched fractions (ICEFs) containing cardioprotective proteins. Accumulation of proteins into ICEFs was PKA dependent and was achieved by ischemic preconditioning or treatment of WT heart with the PDE3 inhibitor cilostamide. Taken together, these findings indicate that PDE3B deletion confers cardioprotective effects because of cAMP/PKA-induced preconditioning, which is associated with the accumulation of proteins with cardioprotective function in ICEFs. To our knowledge, our study is the first to define a role for PDE3B in cardioprotection against I/R injury and suggests PDE3B as a target for cardiovascular therapies.

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Kamel, Rima, Delphine Baetz, Naïg Gueguen, Lucie Lebeau, Agnès Barbelivien, Anne-Laure Guihot, Louwana Allawa, et al. "Kynurenic Acid: A Novel Player in Cardioprotection against Myocardial Ischemia/Reperfusion Injuries." Pharmaceuticals 16, no. 10 (September 28, 2023): 1381. http://dx.doi.org/10.3390/ph16101381.

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Background: Myocardial infarction is one of the leading causes of mortality worldwide; hence, there is an urgent need to discover novel cardioprotective strategies. Kynurenic acid (KYNA), a metabolite of the kynurenine pathway, has been previously reported to have cardioprotective effects. However, the mechanisms by which KYNA may be protective are still unclear. The current study addressed this issue by investigating KYNA’s cardioprotective effect in the context of myocardial ischemia/reperfusion. Methods: H9c2 cells and rats were exposed to hypoxia/reoxygenation or myocardial infarction, respectively, in the presence or absence of KYNA. In vitro, cell death was quantified using flow cytometry analysis of propidium iodide staining. In vivo, TTC-Evans Blue staining was performed to evaluate infarct size. Mitochondrial respiratory chain complex activities were measured using spectrophotometry. Protein expression was evaluated by Western blot, and mRNA levels by RT-qPCR. Results: KYNA treatment significantly reduced H9C2-relative cell death as well as infarct size. KYNA did not exhibit any effect on the mitochondrial respiratory chain complex activity. SOD2 mRNA levels were increased by KYNA. A decrease in p62 protein levels together with a trend of increase in PARK2 may mark a stimulation of mitophagy. Additionally, ERK1/2, Akt, and FOXO3α phosphorylation levels were significantly reduced after the KYNA treatment. Altogether, KYNA significantly reduced myocardial ischemia/reperfusion injuries in both in vitro and in vivo models. Conclusion: Here we show that KYNA-mediated cardioprotection was associated with enhanced mitophagy and antioxidant defense. A deeper understanding of KYNA’s cardioprotective mechanisms is necessary to identify promising novel therapeutic targets and their translation into the clinical arena.

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Barbosa, Roberto Ramos, Taissa Borges Bourguignon, Luíza Dias Torres, Lorenza Silveira Arruda, Tiago de Melo Jacques, Renato Giestas Serpa, Osmar de Araujo Calil, and Luiz Fernando Machado Barbosa. "Anthracycline-associated cardiotoxicity in adults: systematic review on the cardioprotective role of beta-blockers." Revista da Associação Médica Brasileira 64, no. 8 (August 2018): 745–54. http://dx.doi.org/10.1590/1806-9282.64.08.745.

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SUMMARY OBJECTIVES This study aimed at assessing the role of beta-blockers on preventing anthracycline-induced cardiotoxicity in adults. METHODS A systematic review was performed on electronic databases, including relevant studies that analysed beta-blockers as cardioprotective agents before the use of anthracyclines by adult oncologic patients. RESULTS After application of eligibility and selection criteria, eight articles were considered as high quality, complying with the proposed theme; all eight clinical trials, four of them placebo-controlled, with a total number of 655 patients included. From this sample, 281 (42.9%) used beta-blocker as intervention, and carvedilol was the most frequent (167 patients – 25.5%). Six studies were considered positive regarding the cardioprotection role played by beta-blockers, although only four demonstrated significant difference on left ventricle ejection fraction after chemotherapy on groups that used beta-blockers compared to control groups. Carvedilol and nebivolol, but not metoprolol, had positive results regarding cardioprotection. Other beta-blockers were not analysed in the selected studies. CONCLUSIONS Despite the potential cardioprotective effect of beta-blockers, as demonstrated in small and unicentric clinical trials, its routine use on prevention of anthracycline-associated cardiotoxicity demands greater scientific evidence.

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Zhu, Z., P. A. Hofmann, and J. K. Buolamwini. "Cardioprotective effects of novel tetrahydroisoquinoline analogs of nitrobenzylmercaptopurine riboside in an isolated perfused rat heart model of acute myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (June 2007): H2921—H2926. http://dx.doi.org/10.1152/ajpheart.01191.2005.

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We have investigated the cardioprotective effects of novel tetrahydroisoquinoline nitrobenzylmercaptopurine riboside (NBMPR) analog nucleoside transport (NT) inhibitors, compounds 2 and 4, in isolated perfused rat hearts. Langendorff-perfused heart preparations were subjected to 10 min of treatment with compound 2, compound 4, or vehicle (control) followed by 30 min of global ischemia and 120 min of reperfusion. For determination of infarct size, reperfusion time was 180 min. At 1 μM, compounds 2 and 4 provided excellent cardioprotection, with left ventricular developed pressure (LVDP) recovery and end-diastolic pressure (EDP) increase of 82.9 ± 4.0% ( P < 0.001) and 14.1 ± 2.0 mmHg ( P < 0.03) for compound 2-treated hearts and 79.2 ± 5.9% ( P < 0.002) and 7.5 ± 2.7 mmHg ( P < 0.01) for compound 4-treated hearts compared with 41.6 ± 5.2% and 42.5 ± 6.5 mmHg for control hearts. LVDP recovery and EDP increase were 64.1 ± 4.2% and 29.1 ± 2.5 mmHg for hearts treated with 1 μM NBMPR. Compound 4 was the best cardioprotective agent, affording significant cardioprotection, even at 0.1 μM, with LVDP recovery and EDP increase of 76.0 ± 4.9% ( P < 0.003) and 14.1 ± 1.0 mmHg ( P < 0.03). At 1 μM, compound 4 and NBMPR reduced infarct size, with infarct area-to-total risk area ratios of 29.13 ± 3.17 ( P < 0.001) for compound 4 and 37.5 ± 3.42 ( P < 0.01) for NBMPR vs. 51.08 ± 5.06% for control hearts. Infarct size was more effectively reduced by compound 4 than by NBMPR ( P < 0.02). These new tetrahydroisoquinoline NBMPR analogs are not only potent cardioprotective agents but are, also, more effective than NBMPR in this model.

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Das, Samarjit, Istvan Lekli, Manika Das, Gergo Szabo, Judit Varadi, Bela Juhasz, Istvan Bak, et al. "Cardioprotection with palm oil tocotrienols: comparision of different isomers." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (February 2008): H970—H978. http://dx.doi.org/10.1152/ajpheart.01200.2007.

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A recent study from our laboratory indicated the cardioprotective ability of the tocotrienol-rich fraction (TRF) from red palm oil. The present study compared cardioprotective abilities of different isomers of tocotrienol against TRF as recently tocotrienol has been found to function as a potent neuroprotective agent against stroke. Rats were randomly assigned to one of the following groups: animals were given, by gavage, either 0.35%, 1%, or 3.5% TRF for two different periods of time (2 or 4 wk) or 0.03, 0.3, and 3 mg/kg body wt of one of the isomers of tocotrienol (α, γ, or δ) for 4 wk; control animals were given, by gavage, vehicle only. After 2 or 4 wk, rats were killed, and their hearts were then subjected to 30 min of global ischemia followed by 2 h of reperfusion. Dose-response and time-response experiments revealed that the optimal concentration for TRF was 3.5% TRF and 0.3 mg/kg body wt of tocotrienol given for 4 wk. TRF as well as all the isomers of tocotrienol used in our study provided cardioprotection, as evidenced by their ability to improve postischemic ventricular function and reduce myocardial infarct size. The γ-isoform of tocotrienol was the most cardioprotective of all the isomers followed by the α- and δ-isoforms. The molecular mechanisms of cardioprotection afforded by tocotrienol isoforms were probed by evaluating their respective abilities to stabilize the proteasome, allowing it to maintain a balance between prodeath and prosurvival signals. Our results demonstrated that tocotrienol isoforms reduced c-Src but increased the phosphorylation of Akt, thus generating a survival signal.

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Waza, Ajaz Ahmad, Shabir Ahmad Bhat, and Zeenat Hamid. "RELAXIN: A MAGICAL THERAPY FOR HEALTHY HEART." International Journal of Current Pharmaceutical Research 10, no. 1 (January 15, 2018): 1. http://dx.doi.org/10.22159/ijcpr.2018v10i1.24405.

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Relaxin (a peptide hormone) has emerged as a cardioprotective agent and plays a vital role in normal cardiac function. By activation a complex network of signaling cascade, relaxin is responsible for creating a healthy environment for heart functioning. Under pathological conditions, such as cardiomyopathy and heart failure, expression level of relaxin is increased dramatically to protect heart. By promoting angiogenesis, vasodilatation, improving ischemia/reperfusion injury and remodeling, relaxin has emerged as a magical agent to address cardiac abnormalities. Over the past 3 decades, various cardioprotection strategies are in use to deal with cardiac diseases, however till date no effective therapy is in clinical practice. Relaxin has emerged as a novel therapeutic agent to have beneficial action during various pathological conditions. In this review, we have discussed different cardioprotective roles of relaxin that marks it, as an effective agent to tackle heart related diseases.

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Sasali, A., and J. L. Leahy. "Is Metformin Cardioprotective?" Diabetes Care 26, no. 1 (January 1, 2003): 243–44. http://dx.doi.org/10.2337/diacare.26.1.243.

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Williams, Ifor. "Cardioprotective myeloid cells." Science 370, no. 6512 (October 1, 2020): 70.1–70. http://dx.doi.org/10.1126/science.370.6512.70-a.

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Hausenloy, D. J., and D. M. Yellon. "Cardioprotective growth factors." Cardiovascular Research 83, no. 2 (February 13, 2009): 179–94. http://dx.doi.org/10.1093/cvr/cvp062.

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Leenen, Frans H. H., and Balwant S. Tuana. "Cardioprotective Brain Mechanisms." Arteriosclerosis, Thrombosis, and Vascular Biology 32, no. 8 (August 2012): 1749–50. http://dx.doi.org/10.1161/atvbaha.112.252627.

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Wechsler, Andrew S., and Anwar Abd-Elfattah. "Future Cardioprotective Considerations." Journal of Cardiac Surgery 8, no. 4 (July 1993): 492–502. http://dx.doi.org/10.1111/j.1540-8191.1993.tb00400.x.

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Quinlan, Casey L., Alexandre D. T. Costa, and Keith D. Garlid. "The cardioprotective signalosome." Journal of Molecular and Cellular Cardiology 42, no. 6 (June 2007): S47. http://dx.doi.org/10.1016/j.yjmcc.2007.03.132.

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Vis, Annemijn, Jan CAM Lammers, Roel de Vroege, Martijn MJ van Nieuwburg, Marlijn S. Jansen, Joyce MJ Visser, Bart Meuris, Paul F. Gründeman, and Jolanda Kluin. "Strategies to Improve Survival from Surgery for Heart Valve Implantation in Sheep." Comparative Medicine 71, no. 3 (June 1, 2021): 235–39. http://dx.doi.org/10.30802/aalas-cm-20-000118.

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Sheep are a commonly used and validated model for cardiovascular research and, more specifically, for heart valve research. Implanting a heart valve on the arrested heart in sheep is complex and is often complicated by difficulties in restarting the heart, causing significant on-table mortality. Therefore, optimal cardioprotective management during heart valve implantation in sheep is essential. However, little is known about successful cardioprotective management techniques in sheep. This article reports our experience in the cardioprotective management of 20 female sheep that underwent surgical aortic valve replacement with a stented tissue-engineered heart valve prosthesis. During this series of experiments, we modified our cardioprotection protocol to improve survival. We emphasize the importance of total body hypothermia and external cooling of the heart. Furthermore, we recommend repeated cardioplegia administration at 20 min intervals during surgery, with the final dosage of cardioplegia given immediately before the de-clamping of the aorta. To reduce the number of defibrillator shocks during a state of ventricular fibrillation (VF), we have learned to restart the heart by reclamping the aorta, administering cardioplegia until cardiac arrest, and de-clamping the aorta thereafter. Despite these encouraging results, more research is needed to finalize a protocol for this procedure.

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Kim, Ki-Seok, Dennis Abraham, Barbara Williams, Jonathan D. Violin, Lan Mao, and Howard A. Rockman. "β-Arrestin-biased AT1R stimulation promotes cell survival during acute cardiac injury." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 8 (October 15, 2012): H1001—H1010. http://dx.doi.org/10.1152/ajpheart.00475.2012.

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Pharmacological blockade of the ANG II type 1 receptor (AT1R) is a common therapy for treatment of congestive heart failure and hypertension. Increasing evidence suggests that selective engagement of β-arrestin-mediated AT1R signaling, referred to as biased signaling, promotes cardioprotective signaling. Here, we tested the hypothesis that a β-arrestin-biased AT1R ligand TRV120023 would confer cardioprotection in response to acute cardiac injury compared with the traditional AT1R blocker (ARB), losartan. TRV120023 promotes cardiac contractility, assessed by pressure-volume loop analyses, while blocking the effects of endogenous ANG II. Compared with losartan, TRV120023 significantly activates MAPK and Akt signaling pathways. These hemodynamic and biochemical effects were lost in β-arrestin-2 knockout (KO) mice. In response to cardiac injury induced by ischemia reperfusion injury or mechanical stretch, pretreatment with TRV120023 significantly diminishes cell death compared with losartan, which did not appear to be cardioprotective. This cytoprotective effect was lost in β-arrestin-2 KO mice. The β-arrestin-biased AT1R ligand, TRV120023, has cardioprotective and functional properties in vivo, which are distinct from losartan. Our data suggest that this novel class of drugs may provide an advantage over conventional ARBs by supporting cardiac function and reducing cellular injury during acute cardiac injury.

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Zhang, Haitao, Yan Shen, Il-man Kim, Yutao Liu, Jingwen Cai, Adam E. Berman, Kent R. Nilsson, Neal L. Weintraub, and Yaoliang Tang. "Electrical Stimulation Increases the Secretion of Cardioprotective Extracellular Vesicles from Cardiac Mesenchymal Stem Cells." Cells 12, no. 6 (March 11, 2023): 875. http://dx.doi.org/10.3390/cells12060875.

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Clinical trials have shown that electric stimulation (ELSM) using either cardiac resynchronization therapy (CRT) or cardiac contractility modulation (CCM) approaches is an effective treatment for patients with moderate to severe heart failure, but the mechanisms are incompletely understood. Extracellular vesicles (EV) produced by cardiac mesenchymal stem cells (C-MSC) have been reported to be cardioprotective through cell-to-cell communication. In this study, we investigated the effects of ELSM stimulation on EV secretion from C-MSCs (C-MSCELSM). We observed enhanced EV-dependent cardioprotection conferred by conditioned medium (CM) from C-MSCELSM compared to that from non-stimulated control C-MSC (C-MSCCtrl). To investigate the mechanisms of ELSM-stimulated EV secretion, we examined the protein levels of neutral sphingomyelinase 2 (nSMase2), a key enzyme of the endosomal sorting complex required for EV biosynthesis. We detected a time-dependent increase in nSMase2 protein levels in C-MSCELSM compared to C-MSCCtrl. Knockdown of nSMase2 in C-MSC by siRNA significantly reduced EV secretion in C-MSCELSM and attenuated the cardioprotective effect of CM from C-MSCELSM in HL-1 cells. Taken together, our results suggest that ELSM-mediated increases in EV secretion from C-MSC enhance the cardioprotective effects of C-MSC through an EV-dependent mechanism involving nSMase2.

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Journal articles on the topic 'Cardioprotective'

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