Relevant bibliographies by topics / Sodium current, insulin secretion, myocardium

Academic literature on the topic 'Sodium current, insulin secretion, myocardium'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Sodium current, insulin secretion, myocardium"

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Payudis, A. N., O. A. Efremova, L. A. Kamyshnikova, Iu S. Pavlova, O. V. Dudchenko, I. I. Khamnagadaev, and T. P. Golivets. "Effect of SGLT2 inhibitors on the course of chronic heart failure in patients with type 2 diabetes mellitus." Clinician 16, no. 2 (October 10, 2022): 10–16. http://dx.doi.org/10.17650/1818-8338-2022-16-2-k656.

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Diabetes mellitus (DM) is a group of metabolic diseases characterized by chronic hyperglycemia, which is the result of impaired insulin secretion, insulin action, or both. Chronic hyperglycemia in diabetes is accompanied by damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Diabetes mellitus plays a significant role in the formation and is one of the significant risk factors for the development of chronic heart failure (CHF) through its glucose toxic effect, the effect on hyperlipidemia and blood coagulation, impaired autonomic regulation of the heart and a number of other mechanisms. Sodium-glucose cotransporter type 2 (SGLT2) inhibitors are a recently emerging class of antidiabetic drugs that act by inhibiting the reabsorption of glucose in the kidneys. Existing studies of the efficacy and safety of these drugs have shown that they have not only antidiabetic, but also a pronounced organoprotective, especially cardioprotective effect. Today it is believed that the main reason leading to this lies in a decrease in sodium reabsorption in the kidneys, a decrease in the content of intracellular calcium and sodium, and an increase in the concentration of calcium in mitochondria. The role of the ketogenic action of these drugs, their effect on oxidative stress and the processes of inflammation and fibrosis in the myocardium is also considered. The most common side effects of SGLT2 inhibitors include urinary tract and genital infections, euglycemic ketoacidosis. Other possible side effects include an increased risk of lower limb amputations, Fournier gangrene, breast cancer in women, bladder cancer in men, orthostatic hypotension and acute kidney injury, and an increased tendency to fracture. Most side effects can be avoided through adequate patient education and assessment of risk factors and contraindications before starting the use of drugs. Despite the clear need for more research on SGLT2 inhibitors, their widespread use will positively affect the health of the diabetic patient population.
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Braescu, Laurentiu, Marinica Gaspar, Darius Buriman, Oana Maria Aburel, Adrian-Petru Merce, Felix Bratosin, Klokov Sergei Aleksandrovich, Satish Alambaram, and Cristian Mornos. "The Role and Implications of Epicardial Fat in Coronary Atherosclerotic Disease." Journal of Clinical Medicine 11, no. 16 (August 12, 2022): 4718. http://dx.doi.org/10.3390/jcm11164718.

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The current minireview aims to assess the implications of epicardial fat secretory function in the development of coronary artery disease. The epicardial adipose tissue (EAT) is a visceral fat depot that has been described as a cardiovascular risk factor. In addition to its mechanical protection role and physiological secretory function, it seems that various secretion products of the epicardial fat are responsible for metabolic disturbances at the level of the cardiac muscle when in association with pre-existing pathological conditions, such as metabolic syndrome. There is a pathological reduction in sarcomere shortening, abnormal cytosolic Ca2+ fluxes, reduced expression of sarcoplasmic endoplasmic reticulum ATPase 2a and decreased insulin-mediated Akt-Ser473-phosphorylation in association with abnormal levels of epicardial fat tissue. Activin A, angiopoietin-2, and CD14-positive monocytes selectively accumulate in the diseased myocardium, resulting in reduced cardiomyocyte contractile function. At the same time, it is believed that these alterations in secretory products directly decrease the myocyte function via molecular changes, thus contributing to the development of coronary disease when certain comorbidities are associated.
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Aditya, Suruchi, Suryakant Mathur, and Aditya Rattan. "Dapagliflozin: A Novel Therapeutic Approach to Treat Diabetes." JMS SKIMS 14, no. 2 (December 20, 2011): 43–45. http://dx.doi.org/10.33883/jms.v14i2.81.

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Current approaches to treatment of diabetes have many drawbacks. Most of the oral hypoglycemic drugs target the insulin secretion and action. Sodium Glucose co transporters (SGLT)-2 inhibitors are a recent addition to antihyperglycemic drugs that act by reducing glucose reabsorption from the renal filtrate so that bulk of glucose is excreted in the urine. Dapagliflozin, the first in this new class of drugs, is a SGLT2 inhibitor. It causes loss in body weight and is not associated with major hypoglycemic events.Dapagliflozin is currently in advanced development for use alone or in combination with other hypoglycemic agents. Concerns regarding increased cancer risk have delayed the Food and Drug Authority (FDA) approval of this drug. SGLT2 inhibitors represent a major dvancement in management of type 2 diabetes mellitus (T2DM) as they have shifted the focus onto kidney and act independent of insulin. JMS 2011;14(2):43-45
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Serhiyenko, A. A., and V. A. Serhiyenko. "Diabetic cardiomyopathy: treatment." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 16, no. 8 (April 6, 2021): 669–80. http://dx.doi.org/10.22141/2224-0721.16.8.2020.222888.

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This article presents a review of the scientific literature on some key aspects of the current state of the problem of diabetic cardiomyopathy treatment. Measures aimed at reducing insulin resistance, correction of hyperglycemia, dyslipoproteinemia, myocardial metabolism disorders, prevention and treatment of thrombosis, symptomatic therapy of concomitant diseases and syndromes of arterial hypertension, coronary heart disease, heart failure and arrhythmias should be at the forefront of the treatment for diabetic cardiomyopathy. In this direction it is necessary to carry out the following preventive and therapeutic measures: rational nutrition and physical activity; correction of obesity; limiting salt intake to 2–4 g/day; exclusion of smoking, alcohol consumption, products containing caffeine. In particular, the issues are analyzed related to the peculiarities of rational nutrition and physical activity, optimization of glycemic control (insulin and/or insulin secretagogues, glucagon-like peptide-1 analogues, sodium-glucose cotranspor­ter-2 inhibitors); correction of metabolic disorders in the myocar­dium (drugs that improve the energy status of cells — potential means of energy supply for the survival of ischemic myocardium), metabolic modulators (metabolic drugs — trimetazidine, perhexiline, ranolazine; L-carnitine); restriction of extracellular Ca2+ entry into cells (calcium channel blockers), the use of β-adrenergic receptor blockers; modulation of oxidative stress (alpha-lipoic acid, benfotiamine); administration of long-chain ω-3 polyunsaturated fatty acids; sulforaphane, coenzyme Q10; magnesium. Also, promising ways in the treatment of diabetic cardiomyopathy (mimetic peptides for restoring L-type Ca2+ channels; noncoding microRNAs and long noncoding RNAs) are considered.
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Srinivas, Karthik, Melvin George, and Damal Kandadai Sriram. "Empagliflozin: an exciting prospect in the treatment of diabetes." International Journal of Basic & Clinical Pharmacology 7, no. 1 (December 23, 2017): 1. http://dx.doi.org/10.18203/2319-2003.ijbcp20175669.

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Type 2 diabetes mellitus (T2DM) continues to be a chronic and disabling disease that is associated with high mortality and morbidity. The epidemic burden of diabetes mellitus has increased in developing countries and Asia is considered as the “diabetic epicentre”. Type 2 diabetes (T2DM), is characterised by reduced secretion of insulin from pancreatic beta cells independently or associated with reduced response of peripheral tissues to circulating insulin. A proper glycaemic control is essential to delay the micro and macrovascular complications of T2DM. Standard anti-diabetic agents including insulin happen to induce minor to major adverse outcomes in certain populations over prolonged period of administration. Hence there has been a compelling need to develop newer and novel approach to treatment of T2DM. Sodium-glucose co-transporter 2 (SGLT-2) inhibitors are a novel category of drugs that happen to reduce glycaemic overload by inducing glycosuria. The safety, efficacy and tolerability profile of these drugs were studied separately under various trials and was approved for use in August 2014 by US-FDA. This review is an attempt to describe the history of SGLT-2 inhibitors, their mechanism of action, safety and efficacy as well as its current status among anti-diabetic agents.
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Eldesoqui, Mamdouh, Zienab Helmy Eldken, Sally Abdallah Mostafa, Rasha Hamed Al-Serwi, Mohamed El-Sherbiny, Nehal Elsherbiny, Zuhair M. Mohammedsaleh, and Noha Hammad Sakr. "Exercise Augments the Effect of SGLT2 Inhibitor Dapagliflozin on Experimentally Induced Diabetic Cardiomyopathy, Possible Underlying Mechanisms." Metabolites 12, no. 7 (July 11, 2022): 635. http://dx.doi.org/10.3390/metabo12070635.

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One of the most prevalent cardiovascular problems linked with type 2 diabetes mellitus (T2DM) is diabetic cardiomyopathy (DCM). DCM is associated with myocardial oxidative stress, inflammation, apoptosis, suppressed autophagy, extracellular matrix remodeling, and fibrosis. The current study aims to investigate the protective effect of sodium-glucose transport 2 inhibitor (SGLT2i) dapagliflozin and/or exercise on DCM. Thirty adult male Sprague Dawley rats are used. T2DM is induced by a 6-week high-fat diet (HFD) followed by a single intraperitoneal (IP) injection of 35 mg/kg streptozotocin (STZ). Rats are divided into five groups, control, diabetic (DM), DM + swimming, DM + dapagliflozin, and DM + dapagliflozin and swimming. Serum glucose, insulin, insulin resistance (HOMA-IR), and cardiac enzymes (CK-MB and lactate dehydrogenase (LDH) are measured. Heart specimens are used for evaluation of cellular oxidative stress markers malondialdehyde (MDA), antioxidant enzymes, glutathione (GSH), and catalase (CAT), as well as mRNA expression of TGF-β, MMP9, IL-1β, and TNF-α. Stained sections with haematoxylin and eosin (H & E) and Masson trichrome are used for histopathological evaluation and detection of fibrosis, respectively. Immunohistochemical staining for apoptosis (caspase-3), and autophagy (LC3) are also carried out. The combinations of SGLT2i and exercise exhibited the most significant cardioprotective effect. It improved diabetic-induced histopathological alterations in the myocardium and attenuated the elevation of serum blood glucose, CK-MB, LDH, myocardial MDA, and mRNA expression of TNF-α, IL-1β, TGF-β, MMP9, and the immune expression of caspase-3. Moreover, this combination increased the serum insulin, myocardial antioxidants GSH and CAT, and increase the immune expression of the LC-3. In conclusion, a combination of SGLT2i and exercise exerted a better antioxidant, anti-inflammatory, and antifibrotic effect in DCM. Moreover, the combination enhances the autophagic capacity of the heart.
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Soldatov, Vladislav O., Elena A. Shmykova, Marina A. Pershina, Andrey O. Ksenofontov, Yaroslav M. Zamitsky, Alexandr L. Kulikov, Anna A. Peresypkina, Anton P. Dovgan, and Yuliya V. Belousova. "Imidazoline receptors agonists: possible mechanisms of endothelioprotection." Research Results in Pharmacology 4, no. 2 (July 19, 2018): 11–19. http://dx.doi.org/10.3897/rrpharmacology.4.27221.

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Imidazoline receptor agonists are one of the groups of contemporary antihypertensive drugs with the pleiotropic cardiovascular effects. In this review, the historical, physiological, pathophysiological aspects concerning imidazoline receptor agonists and possible mechanisms for their participation in endothelioprotection were considered. Illuminated the molecular biology of each subtype of imidazoline receptors and their significance in the pharmacological correction of cardiovascular disease. IR type 1 are localized in the brain nucleus, carrying out the descending tonic control of sympathetic activation, as well as in the endothelial cells of the vessels and kidneys. Their activation leads to a decrease in blood pressure, slowing the remodeling of the vascular wall and increasing sodium nares. IR type 2 is expressed predominantly in the adrenal gland, fat and muscle tissues. The physiological effects of their stimulation are associated with an increase in glucose utilization by peripheral tissues. IR type 3 are mainly present in pancreatic cells and are associated with the regulation of insulin secretion. Their stimulation leads to an increase in insulin liberation. Thus, IR agonists are able to improve endothelial function through various mechanisms, including blood pressure reduction, improvement in metabolic profile, and direct positive effects on the vascular wall. Current information on the pharmacological effects of this group compounds allows us to conclude that they are a promising group for correcting endothelial dysfunction and complications associated with it.
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8

Wang, Guangju, Xiumei Li, Ying Zhou, Jinghai Feng, and Minhong Zhang. "Effects of Dietary Chromium Picolinate on Gut Microbiota, Gastrointestinal Peptides, Glucose Homeostasis, and Performance of Heat-Stressed Broilers." Animals 12, no. 7 (March 27, 2022): 844. http://dx.doi.org/10.3390/ani12070844.

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The current research was devoted to evaluating the effects on gut microbiota, gastrointestinal peptides, and glucose homeostasis of chromium picolinate applied to heat-stressed broilers. In a 14 d experiment, 220 28-day-old AA broilers were randomly assigned into one thermal-neutral and three high-temperature groups dietary-supplemented with 0, 0.4, or 0.8 mg/kg of chromium as chromium picolinate. The temperature for the thermal-neutral group was set at 21 °C, while that for the other three groups (high temperature) was set at 31 °C. The results showed that the average daily gain and average daily feed intake of the 0.4 mg/kg chromium-supplemented group significantly increased compared with the high-temperature groups (p < 0.05). The content of cholecystokinin in the 0.4 mg/kg group significantly decreased, and the gastric inhibitory polypeptide level was significantly elevated in jejunum (p < 0.05). The cecal microbiota of heat-stressed broilers was substantially different from that of the thermal-neutral group. After diet-supplemented chromium, compared to the high-temperature groups, the 0.4 mg/kg chromium supplemented group was characterized by a reduction of Actinobacteriota and Proteobacteria at the phylum level. The Bacilli were elevated, while proportions of Coriobacteria and Gammaproteobacteria were reduced significantly at the class level. The proportions of Lactobacillaceae, Christensenellaceae, and Erysipelotrichaceae were elevated significantly, while that of Clostridiaceae was reduced significantly at the family level. The proportion of Turicibacter was elevated significantly and the proportions of Olsenella and Ruminococcus were reduced significantly at the genus level (p < 0.05). Compared to the high-temperature groups, in the 0.4 mg/kg chromium-supplemented group, the insulin concentration and insulin resistance index were reduced (p < 0.05), and sodium-glucose transporter 1 expression was up-regulated in jejunum (p < 0.05). Performance, microbiota, gastrointestinal peptides, or serum parameters of the 0.8 mg/kg group were almost unaffected by chromium compared with the high-temperature groups. In conclusion, diet supplemented with 0.4 mg/kg Cr improved performance, insulin resistance and sodium-glucose transporter 1 expression and altered gut microflora structure and secretion of gastrointestinal peptides, thus showing that supplementation with chromium is beneficial to maintain glucose homeostasis and alleviate heat stress.
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9

Bergman, E. N. "Energy contributions of volatile fatty acids from the gastrointestinal tract in various species." Physiological Reviews 70, no. 2 (April 1, 1990): 567–90. http://dx.doi.org/10.1152/physrev.1990.70.2.567.

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The VFA, also known as short-chain fatty acids, are produced in the gastrointestinal tract by microbial fermentation of carbohydrates and endogenous substrates, such as mucus. This can be of great advantage to the animal, since no digestive enzymes exist for breaking down cellulose or other complex carbohydrates. The VFA are produced in the largest amounts in herbivorous animal species and especially in the forestomach of ruminants. The VFA, however, also are produced in the lower digestive tract of humans and all animal species, and intestinal fermentation resembles that occurring in the rumen. The principal VFA in either the rumen or large intestine are acetate, propionate, and butyrate and are produced in a ratio varying from approximately 75:15:10 to 40:40:20. Absorption of VFA at their site of production is rapid, and large quantities are metabolized by the ruminal or large intestinal epithelium before reaching the portal blood. Most of the butyrate is converted to ketone bodies or CO2 by the epithelial cells, and nearly all of the remainder is removed by the liver. Propionate is similarly removed by the liver but is largely converted to glucose. Although species differences exist, acetate is used principally by peripheral tissues, especially fat and muscle. Considerable energy is obtained from VFA in herbivorous species, and far more research has been conducted on ruminants than on other species. Significant VFA, however, are now known to be produced in omnivorous species, such as pigs and humans. Current estimates are that VFA contribute approximately 70% to the caloric requirements of ruminants, such as sheep and cattle, approximately 10% for humans, and approximately 20-30% for several other omnivorous or herbivorous animals. The amount of fiber in the diet undoubtedly affects the amount of VFA produced, and thus the contribution of VFA to the energy needs of the body could become considerably greater as the dietary fiber increases. Pigs and some species of monkey most closely resemble humans, and current research should be directed toward examining the fermentation processes and VFA metabolism in those species. In addition to the energetic or nutritional contributions of VFA to the body, the VFA may indirectly influence cholesterol synthesis and even help regulate insulin or glucagon secretion. In addition, VFA production and absorption have a very significant effect on epithelial cell growth, blood flow, and the normal secretory and absorptive functions of the large intestine, cecum, and rumen. The absorption of VFA and sodium, for example, seem to be interdependent, and release of bicarbonate usually occurs during VFA absorption.(ABSTRACT TRUNCATED AT 400 WORDS)
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10

Andre, E., E. Yaniz-Galende, C. Hamilton, G. J. Dusting, N. Hellen, CE Poulet, M. Diez Cunado, et al. "Poster session 1Cell growth, differentiation and stem cells - Heart72Understanding the metabolism of cardiac progenitor cells: a first step towards controlling their proliferation and differentiation?73Expression of pw1/peg3 identifies a new cardiac adult stem cell population involved in post-myocardial infarction remodeling74Long-term stimulation of iPS-derived cardiomyocytes using optogenetic techniques to promote phenotypic changes in E-C coupling75Benefits of electrical stimulation on differentiation and maturation of cardiomyocytes from human induced pluripotent stem cells76Constitutive beta-adrenoceptor-mediated cAMP production controls spontaneous automaticity of human induced pluripotent stem cell-derived cardiomyocytes77Formation and stability of T-tubules in cardiomyocytes78Identification of miRNAs promoting human cardiomyocyte proliferation by regulating Hippo pathway79A direct comparison of foetal to adult epicardial cell activation reveals distinct differences relevant for the post-injury response80Role of neuropilins in zebrafish heart regeneration81Highly efficient immunomagnetic purification of cardiomyocytes derived from human pluripotent stem cells82Cardiac progenitor cells posses a molecular circadian clock and display large 24-hour oscillations in proliferation and stress tolerance83Influence of sirolimus and everolimus on bone marrow-derived mesenchymal stem cell biology84Endoglin is important for epicardial behaviour following cardiac injuryCell death and apoptosis - Heart87Ultrastructural alterations reflecting Ca2+ handling and cell-to-cell coupling disorders precede occurrence of severe arrhythmias in intact animal heart88Urocortin-1 promotes cardioprotection through ERK1/2 and EPAC pathways: role in apoptosis and necrosis89Expression p38 MAPK and Cas-3 in myocardium LV of rats with experimental heart failure at melatonin and enalapril introductionTranscriptional control and RNA species - Heart92Accumulation of beta-amyloid 1-40 in HF patients: the role of lncRNA BACE1-AS93Role of miR-182 in zebrafish and mouse models of Holt-Oram syndrome94Mir-27 distinctly regulates muscle-enriched transcription factors and growth factors in cardiac and skeletal muscle cells95AF risk factors impair PITX2 expression leading to Wnt-microRNA-ion channel remodelingCytokines and cellular inflammation - Heart98Post-infarct survival depends on the interplay of monocytes, neutrophils and interferon gamma in a mouse model of myocardial Infarction99Inflammatory cd11b/c cells play a protective role in compensated cardiac hypertrophy by promoting an orai3-related pro-survival signal100Anti-inflammatory effects of endothelin receptor blockade in the atrial tissue of spontaneously hypertensive rats101Mesenchymal stromal cells reduce NLRP3 inflammasome activity in Coxsackievirus B3-induced myocarditis102Mesenchymal stromal cells modulate monocytes trafficking in Coxsackievirus B3-induced myocarditis103The impact of regulatory T lymphocytes on long-term mortality in patients with chronic heart failure104Temporal dynamics of dendritic cells after ST-elevation myocardial infarction relate with improvement of myocardial functionGrowth factors and neurohormones - Heart107Preconditioning of hypertrophied heart: miR-1 and IGF-1 crosstalk108Modulation of catecholamine secretion from human adrenal chromaffin cells by manipulation of G protein-coupled receptor kinase-2 activity109Evaluation of cyclic adenosin-3,5- monophosphate and neurohormones in patients with chronic heart failureNitric oxide and reactive oxygen species - Heart112Hydrogen sulfide donor inhibits oxidative and nitrosative stress, cardiohemodynamics disturbances and restores cNOS coupling in old rats113Role and mechanisms of action of aldehydes produced by monoamine oxidase A in cardiomyocyte death and heart failure114Exercise training has contrasting effects in myocardial infarction and pressure-overload due to different endothelial nitric oxide synthase regulation115S-Nitroso Human Serum Albumin dose-dependently leads to vasodilation and alters reactive hyperaemia in coronary arteries of an isolated mouse heart model116Modulating endothelial nitric oxide synthase with folic acid attenuates doxorubicin-induced cardiomyopathy119Effects of long-term very high intensity exercise on aortic structure and function in an animal model120Electron paramagnetic resonance spectroscopy quantification of nitrosylated hemoglobin (HbNO) as an index of vascular nitric oxide bioavailability in vivo121Deletion of repressor activator protein 1 impairs acetylcholine-induced relaxation due to production of reactive oxygen speciesExtracellular matrix and fibrosis - Heart124MicroRNA-19b is associated with myocardial collagen cross-linking in patients with severe aortic stenosis. Potential usefulness as a circulating biomarker125A new ex vivo model to study cardiac fibrosis126Heterogeneity of fibrosis and fibroblast differentiation in the left ventricle after myocardial infarction127Effect of carbohydrate metabolism degree compensation to the level of galectin-3 changes in hypertensive patients with chronic heart failure and type 2 diabetes mellitus128Statin paradox in association with calcification of bicuspid aortic valve interstitial cells129Cardiac function remains impaired despite reversible cardiac fibrosis after healed experimental viral myocarditisIon channels, ion exchangers and cellular electrophysiology - Heart132Identifying a novel role for PMCA1 (Atp2b1) in heart rhythm instability133Mutations of the caveolin-3 gene as a predisposing factor for cardiac arrhythmias134The human sinoatrial node action potential: time for a computational model135iPSC-derived cardiomyocytes as a model to dissect ion current alterations of genetic atrial fibrillation136Postextrasystolic potentiation in healthy and diseased hearts: effects of the site of origin and coupling interval of the preceding extrasystole137Absence of Nav1.8-based (late) sodium current in rabbit cardiomyocytes and human iPSC-CMs138hiPSC-derived cardiomyocytes from Brugada Syndrome patients without identified mutations do not exhibit cellular electrophysiological abnormalitiesMicrocirculation141Atherogenic indices, collagen type IV turnover and the development of microvascular complications- study in diabetics with arterial hypertension142Changes in the microvasculature and blood viscosity in women with rheumatoid arthritis, hypercholesterolemia and hypertensionAtherosclerosis145Shear stress regulates endothelial autophagy: consequences on endothelial senescence and atherogenesis146Obstructive sleep apnea causes aortic remodeling in a chronic murine model147Aortic perivascular adipose tissue displays an aged phenotype in early and late atherosclerosis in ApoE-/- mice148A systematic evaluation of the cellular innate immune response during the process of human atherosclerosis149Inhibition of Coagulation factor Xa increases plaque stability and attenuates the onset and progression of atherosclerotic plaque in apolipoprotein e-deficient mice150Regulatory CD4+ T cells from patients with atherosclerosis display pro-inflammatory skewing and enhanced suppression function151Hypoxia-inducible factor (HIF)-1alpha regulates macrophage energy metabolism by mediating miRNAs152Extracellular S100A4 is a key player of smooth muscle cell phenotypic transition: implications in atherosclerosis153Microparticles of healthy origins improve atherosclerosis-associated endothelial progenitor cell dysfunction via microRNA transfer154Arterial remodeling and metabolism impairment in early atherosclerosis155Role of pannexin1 in atherosclerotic plaque formationCalcium fluxes and excitation-contraction coupling158Amphiphysin II induces tubule formation in cardiac cells159Interleukin 1 beta regulation of connexin 43 in cardiac fibroblasts and the effects of adult cardiac myocyte:fibroblast co-culture on myocyte contraction160T-tubular electrical defects contribute to blunted beta-adrenergic response in heart failure161Beat-to-beat variability of intracellular Ca2+ dynamics of Purkinje cells in the infarct border zone of the mouse heart revealed by rapid-scanning confocal microscopy162The efficacy of late sodium current blockers in hypertrophic cardiomyopathy is dependent on genotype: a study on transgenic mouse models with different mutations163Synthesis of cADPR and NAADP by intracellular CD38 in heart: role in inotropic and arrhythmogenic effects of beta-adrenoceptor signalingContractile apparatus166Towards an engineered heart tissue model of HCM using hiPSC expressing the ACTC E99K mutation167Diastolic mechanical load delays structural and functional deterioration of ultrathin adult heart slices in culture168Structural investigation of the cardiac troponin complex by molecular dynamics169Exercise training restores myocardial and oxidative skeletal muscle function from myocardial infarction heart failure ratsOxygen sensing, ischaemia and reperfusion172A novel antibody specific to full-length stromal derived factor-1 alpha reveals that remote conditioning induces its cleavage by endothelial dipeptidyl peptidase 4173Attenuation of myocardial and vascular arginase activity by vagal nerve stimulation via a mechanism involving alpha-7 nicotinic receptor during cardiac ischemia and reperfusion174Novel nanoparticle-mediated medicine for myocardial ischemia-reperfusion injury simultaneously targeting mitochondrial injury and myocardial inflammation175Acetylcholine plays a key role in myocardial ischaemic preconditioning via recruitment of intrinsic cardiac ganglia176The role of nitric oxide and VEGFR-2 signaling in post ischemic revascularization and muscle recovery in aged hypercholesterolemic mice177Efficacy of ischemic preconditioning to protect the human myocardium: the role of clinical conditions and treatmentsCardiomyopathies and fibrosis180Plakophilin-2 haploinsufficiency leads to impaired canonical Wnt signaling in ARVC patient181Improved technique for customized, easier, safer and more reliable transverse aortic arch banding and debanding in mice as a model of pressure overload hypertrophy182Late sodium current inhibitors for the treatment of inducible obstruction and diastolic dysfunction in hypertrophic cardiomyopathy: a study on human myocardium183Angiotensin II receptor antagonist fimasartan has protective role of left ventricular fibrosis and remodeling in the rat ischemic heart184Role of High-Mobility Group Box 1 (HMGB1) redox state on cardiac fibroblasts activities and heart function after myocardial infarction185Atrial remodeling in hypertrophic cardiomyopathy: insights from mouse models carrying different mutations in cTnT186Electrophysiological abnormalities in ventricular cardiomyocytes from a Maine Coon cat with hypertrophic cardiomyopathy: effects of ranolazine187ZBTB17 is a novel cardiomyopathy candidate gene and regulates autophagy in the heart188Inhibition of SRSF4 in cardiomyocytes induces left ventricular hypertrophy189Molecular characterization of a novel cardiomyopathy related desmin frame shift mutation190Autonomic characterisation of electro-mechanical remodeling in an in-vitro leporine model of heart failure191Modulation of Ca2+-regulatory function by three novel mutations in TNNI3 associated with severe infant restrictive cardiomyopathyAging194The aging impact on cardiac mesenchymal like stromal cells (S+P+)195Reversal of premature aging markers after bariatric surgery196Sex-associated differences in vascular remodeling during aging: role of renin-angiotensin system197Role of the receptor for advanced glycation end-products (RAGE) in age dependent left ventricle dysfunctionsGenetics and epigenetics200hsa-miR-21-5p as a key factor in aortic remodeling during aneurysm formation201Co-inheritance of mutations associated with arrhythmogenic and hypertrophic cardiomyopathy in two Italian families202Lamin a/c hot spot codon 190: form various amino acid substitutions to clinical effects203Treatment with aspirin and atorvastatin attenuate cardiac injury induced by rat chest irradiation: Implication of myocardial miR-1, miR-21, connexin-43 and PKCGenomics, proteomics, metabolomics, lipidomics and glycomics206Differential phosphorylation of desmin at serines 27 and 31 drives the accumulation of preamyloid oligomers in heart failure207Potential role of kinase Akt2 in the reduced recovery of type 2 diabetic hearts subjected to ischemia / reperfusion injury208A proteomics comparison of extracellular matrix remodelling in porcine coronary arteries upon stent implantationMetabolism, diabetes mellitus and obesity211Targeting grk2 as therapeutic strategy for cancer associated to diabetes212Effects of salbutamol on large arterial stiffness in patients with metabolic syndrome213Circulating microRNA-1 and microRNA-133a: potential biomarkers of myocardial steatosis in type 2 diabetes mellitus214Anti-inflammatory nutrigenomic effects of hydroxytyrosol in human adipocytes - protective mechanisms of mediterranean diets in obesity-related inflammation215Alterations in the metal content of different cardiac regions within a rat model of diabetic cardiomyopathyTissue engineering218A novel conductive patch for application in cardiac tissue engineering219Establishment of a simplified and improved workflow from neonatal heart dissociation to cardiomyocyte purification and characterization220Effects of flexible substrate on cardiomyocytes cell culture221Mechanical stretching on cardiac adipose progenitors upregulates sarcomere-related genes." Cardiovascular Research 111, suppl 1 (July 1, 2016): S16—S42. http://dx.doi.org/10.1093/cvr/cvw135.

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Dissertations / Theses on the topic "Sodium current, insulin secretion, myocardium"

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RIZZETTO, RICCARDO. "Pathophysiology of the late sodium current: from myocardium to pancreatic beta cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/43677.

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The sustained component of the sodium current (INaL) has been recently found enhanced in several cardiac pathologies. INaL enhancement has been highlighted as a major cause of cellular dysfunction, caused by INaL-dependent electrical instability (arrythmias) and alterations in intracellular ions (Na and Ca) homeostasis. Recent evidence of beneficial effects of the INaL blocker ranolazine (RAN) in diabetes motivates interest in the role of the INaL in glucose-induced insulin secretion (GSIS). The aim of the present thesis is to characterize INaL, identified as steady-state current blocked by RAN (IRAN) or TTX (ITTX), and its function in rat INS-1E cells and human islet cells (HIc). Veratridine (VERA) was used as INaL enhancer. Baseline INaL was similar between INS-1E and HIc. In INS-1E cells, tolbutamide-triggered action potentials were suppressed by TTX, but not by RAN. VERA caused depolarization, countered by INaL blockade. ITTX and IRAN reversal potentials (EREV) were negative to Na+ equilibrium one, but they approached it when K+-channels were blocked. This revealed INaL coupling to Na+-activated K+ current (IKNa); expression of IKNa channels (Slo2.1/2.2) was confirmed by transcript analysis. Concomitant activation of IKNa might blunt the effects of INaL on membrane potential, but at the same time it might increase the impact of INaL on intracellular Ca2+. Consistently, INaL blockade (by TTX) blunted cytosolic Ca2+ response to depolarization, with the highest effect in the intermediate potentials. Long-term exposure to 33 mM glucose (CHG) enhanced INaL. Whereas acute INaL enhancement (VERA) increased GSIS, chronic one (CHG or VERA) depressed GSIS, which was partially restored by RAN. Conclusions: 1) INaL is expressed in insulin-secreting cells, is coupled to IKNa, affects Ca2+ signalling and, when enhanced acutely, increases GSIS 2) sustained hyperglycemic stress enhances INaL and this contributes to GSIS depression instead. Overall, INaL enhancement may represent a common mechanism contributing to disease progression in cardiac and secretion disorders.
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