Journal articles: 'Heart development'

1

Leinwand, Leslie A. "Heart Development." Nature Medicine 5, no. 3 (March 1999): 260. http://dx.doi.org/10.1038/6466.

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2

Kiberstis, P. A. "DEVELOPMENT: Orchestrating a Heart-to-Heart." Science 289, no. 5479 (July 28, 2000): 509b—509. http://dx.doi.org/10.1126/science.289.5479.509b.

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3

Combs, Michelle D., and Katherine E. Yutzey. "Heart Valve Development." Circulation Research 105, no. 5 (August 28, 2009): 408–21. http://dx.doi.org/10.1161/circresaha.109.201566.

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4

Lyons, Gary E. "Vertebrate heart development." Current Opinion in Genetics & Development 6, no. 4 (August 1996): 454–60. http://dx.doi.org/10.1016/s0959-437x(96)80067-0.

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5

Armstrong, Ehrin J., and Joyce Bischoff. "Heart Valve Development." Circulation Research 95, no. 5 (September 3, 2004): 459–70. http://dx.doi.org/10.1161/01.res.0000141146.95728.da.

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6

Schleich, J.-M. "Development of the human heart: days 15-21." Heart 87, no. 5 (May 1, 2002): 487. http://dx.doi.org/10.1136/heart.87.5.487.

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Anderson, R. H. "Development and structure of the atrial septum." Heart 88, no. 1 (July 1, 2002): 104–10. http://dx.doi.org/10.1136/heart.88.1.104.

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Houyel, Lucile, and Sigolène M. Meilhac. "Heart Development and Congenital Structural Heart Defects." Annual Review of Genomics and Human Genetics 22, no. 1 (August 31, 2021): 257–84. http://dx.doi.org/10.1146/annurev-genom-083118-015012.

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Congenital heart disease is the most frequent birth defect and the leading cause of death for the fetus and in the first year of life. The wide phenotypic diversity of congenital heart defects requires expert diagnosis and sophisticated repair surgery. Although these defects have been described since the seventeenth century, it was only in 2005 that a consensus international nomenclature was adopted, followed by an international classification in 2017 to help provide better management of patients. Advances in genetic engineering, imaging, and omics analyses have uncovered mechanisms of heart formation and malformation in animal models, but approximately 80% of congenital heart defects have an unknown genetic origin. Here, we summarize current knowledge of congenital structural heart defects, intertwining clinical and fundamental research perspectives, with the aim to foster interdisciplinary collaborations at the cutting edge of each field. We also discuss remaining challenges in better understanding congenital heart defects and providing benefits to patients.

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Sun, Dong, An Huang, Gong Zhao, Robert Bernstein, Paul Forfia, Xiaobin Xu, Akos Koller, Gabor Kaley, and Thomas H. Hintze. "Reduced NO-dependent arteriolar dilation during the development of cardiomyopathy." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (February 1, 2000): H461—H468. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h461.

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Our previous studies have suggested that there is reduced nitric oxide (NO) production in canine coronary blood vessels after the development of pacing-induced heart failure. The goal of these studies was to determine whether flow-induced NO-mediated dilation is altered in coronary arterioles during the development of heart failure. Subepicardial coronary arterioles (basal diameter 80 μm) were isolated from normal canine hearts, from hearts with dysfunction but no heart failure, and from hearts with severe cardiac decompensation. Arterioles were perfused at increasing flow or administered agonists with no flow in vitro. In arterioles from normal hearts, flow increased arteriolar diameter, with one-half of the response being NO dependent and one-half prostaglandin dependent. Shear stress-induced dilation was eliminated by removing the endothelium. Arterioles from normal hearts and hearts with dysfunction but no failure responded to increasing shear stress with dilation that reached a maximum at a shear stress of 20 dyn/cm2. In contrast, arterioles from failing hearts showed a reduced dilation, reaching only 55% of the dilation seen in vessels of normal hearts at a shear stress of 100 dyn/cm2. This remaining dilation was eliminated by indomethacin, suggesting that the NO-dependent component was absent in coronary microvessels after the development of heart failure. Similarly, agonist-induced NO-dependent coronary arteriolar dilation was markedly attenuated after the development of heart failure. After the development of severe dilated cardiomyopathy and heart failure, the NO-dependent component of both shear stress- and agonist-induced arteriolar dilation is reduced or entirely absent.

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10

Mustroph, Julian, Can M. Sag, Felix Bähr, Anna-Lena Schmidtmann, Shamindra N. Gupta, Alexander Dietz, M. M. Towhidul Islam, et al. "Loss of CASK Accelerates Heart Failure Development." Circulation Research 128, no. 8 (April 16, 2021): 1139–55. http://dx.doi.org/10.1161/circresaha.120.318170.

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Rationale: Increased myocardial activity of CaMKII (Ca/calmodulin-dependent kinase II) leads to heart failure and arrhythmias. In Drosophila neurons, interaction of CaMKII with CASK (Ca/CaM-dependent serine protein kinase) has been shown to inhibit CaMKII activity, but the consequences of this regulation for heart failure and ventricular arrhythmias are unknown. Objective: We hypothesize that CASK associates with CaMKII in human and mouse hearts thereby limiting CaMKII activity and that altering CASK expression in mice changes CaMKII activity accordingly, with functional consequences for contractile function and arrhythmias. Methods and Results: Immunoprecipitation revealed that CASK associates with CaMKII in human hearts. CASK expression is unaltered in heart failure but increased in patients with aortic stenosis. In mice, cardiomyocyte-specific knockout of CASK increased CaMKII-autophosphorylation at the stimulatory T287 site, but reduced phosphorylation at the inhibitory T305/306 site. Knockout of CASK mice showed increased CaMKII-dependent sarcoplasmic reticulum Ca leak, reduced sarcoplasmic reticulum Ca content, increased susceptibility to ventricular arrhythmias, greater loss of ejection fraction, and increased mortality after transverse aortic constriction. Intriguingly, stimulation of the cardiac glucagon-like peptide 1 receptor with exenatide increased CASK expression resulting in increased inhibitory CaMKII T305 phosphorylation, reduced CaMKII activity, and reduced sarcoplasmic reticulum Ca leak in wild type but not CASK-KO. Conclusions: CASK associates with CaMKII in the human heart. Knockout of CASK in mice increases CaMKII activity, leading to contractile dysfunction and arrhythmias. Increasing CASK expression reduces CaMKII activity, improves Ca handling and contractile function.

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11

LIU, Yang, LiXiang XUE, Jun LI, and Han LU. "Polycomb and Heart Development." SCIENTIA SINICA Vitae 45, no. 7 (July 1, 2015): 643–51. http://dx.doi.org/10.1360/n052015-00026.

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12

Cao, Yingxi, Sierra Duca, and Jingli Cao. "Epicardium in Heart Development." Cold Spring Harbor Perspectives in Biology 12, no. 2 (August 26, 2019): a037192. http://dx.doi.org/10.1101/cshperspect.a037192.

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13

Pickersgill, H. "DEVELOPMENT: Hand Over Heart." Science 323, no. 5912 (January 16, 2009): 310a. http://dx.doi.org/10.1126/science.323.5912.310a.

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14

Anderson, Page A. W. "The heart and development." Seminars in Perinatology 20, no. 6 (December 1996): 482–509. http://dx.doi.org/10.1016/s0146-0005(96)80064-4.

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15

Tao, Ye, and Robert A. Schulz. "Heart development in Drosophila." Seminars in Cell & Developmental Biology 18, no. 1 (February 2007): 3–15. http://dx.doi.org/10.1016/j.semcdb.2006.12.001.

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16

Chen, J. "Genetics of heart development." Trends in Genetics 16, no. 9 (September 1, 2000): 383–88. http://dx.doi.org/10.1016/s0168-9525(00)02075-8.

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17

Chatterjee, Bishwanath. "Heart Development and Regeneration." Journal of Cardiovascular Disease Research 2, no. 2 (April 2011): 137–38. http://dx.doi.org/10.1016/s0975-3583(11)22011-4.

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18

Nakajima, Yuji, Masahide Sakabe, Hiroko Matsui, Hirokazu Sakata, Nariaki Yanagawa, and Toshiyuki Yamagishi. "Heart development before beating." Anatomical Science International 84, no. 3 (March 4, 2009): 67–76. http://dx.doi.org/10.1007/s12565-009-0025-2.

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19

Lough, John, and Yukiko Sugi. "Endoderm and heart development." Developmental Dynamics 217, no. 4 (April 2000): 327–42. http://dx.doi.org/10.1002/(sici)1097-0177(200004)217:4<327::aid-dvdy1>3.0.co;2-k.

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20

Opitz, John M., and Edward B. Clark. "Heart development: An introduction." American Journal of Medical Genetics 97, no. 4 (2000): 238–47. http://dx.doi.org/10.1002/1096-8628(200024)97:4<238::aid-ajmg1274>3.0.co;2-g.

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21

Bowthorpe, Meaghan, Vincent Castonguay-Siu, and Mahdi Tavakoli. "Development of a Robotic System to Enable Beating-heart Surgery." Journal of the Robotics Society of Japan 32, no. 4 (2014): 339–46. http://dx.doi.org/10.7210/jrsj.32.339.

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22

Pederson, Bartholomew A., Hanying Chen, Jill M. Schroeder, Weinian Shou, Anna A. DePaoli-Roach, and Peter J. Roach. "Abnormal Cardiac Development in the Absence of Heart Glycogen." Molecular and Cellular Biology 24, no. 16 (August 15, 2004): 7179–87. http://dx.doi.org/10.1128/mcb.24.16.7179-7187.2004.

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ABSTRACT Glycogen serves as a repository of glucose in many mammalian tissues. Mice lacking this glucose reserve in muscle, heart, and several other tissues were generated by disruption of the GYS1 gene, which encodes an isoform of glycogen synthase. Crossing mice heterozygous for the GYS1 disruption resulted in a significant underrepresentation of GYS1-null mice in the offspring. Timed matings established that Mendelian inheritance was followed for up to 18.5 days postcoitum (dpc) and that ∼90% of GYS1-null animals died soon after birth due to impaired cardiac function. Defects in cardiac development began between 11.5 and 14.5 dpc. At 18.5 dpc, the hearts were significantly smaller, with reduced ventricular chamber size and enlarged atria. Consistent with impaired cardiac function, edema, pooling of blood, and hemorrhagic liver were seen. Glycogen synthase and glycogen were undetectable in cardiac muscle and skeletal muscle from the surviving null mice, and the hearts showed normal morphology and function. Congenital heart disease is one of the most common birth defects in humans, at up to 1 in 50 live births. The results provide the first direct evidence that the ability to synthesize glycogen in cardiac muscle is critical for normal heart development and hence that its impairment could be a significant contributor to congenital heart defects.

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23

Anderson, R. H. "Development of the heart: (2) Septation of the atriums and ventricles." Heart 89, no. 8 (August 1, 2003): 949–58. http://dx.doi.org/10.1136/heart.89.8.949.

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24

Lansford, Rusty, and Sandra Rugonyi. "Follow Me! A Tale of Avian Heart Development with Comparisons to Mammal Heart Development." Journal of Cardiovascular Development and Disease 7, no. 1 (March 7, 2020): 8. http://dx.doi.org/10.3390/jcdd7010008.

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Avian embryos have been used for centuries to study development due to the ease of access. Because the embryos are sheltered inside the eggshell, a small window in the shell is ideal for visualizing the embryos and performing different interventions. The window can then be covered, and the embryo returned to the incubator for the desired amount of time, and observed during further development. Up to about 4 days of chicken development (out of 21 days of incubation), when the egg is opened the embryo is on top of the yolk, and its heart is on top of its body. This allows easy imaging of heart formation and heart development using non-invasive techniques, including regular optical microscopy. After day 4, the embryo starts sinking into the yolk, but still imaging technologies, such as ultrasound, can tomographically image the embryo and its heart in vivo. Importantly, because like the human heart the avian heart develops into a four-chambered heart with valves, heart malformations and pathologies that human babies suffer can be replicated in avian embryos, allowing a unique developmental window into human congenital heart disease. Here, we review avian heart formation and provide comparisons to the mammalian heart.

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25

Cooley, Denton A. "Early Development of Congenital Heart Surgery: Open Heart Procedures." Annals of Thoracic Surgery 64, no. 5 (November 1997): 1544–48. http://dx.doi.org/10.1016/s0003-4975(97)01025-4.

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26

Martin, Kendall E., and Joshua S. Waxman. "Atrial and Sinoatrial Node Development in the Zebrafish Heart." Journal of Cardiovascular Development and Disease 8, no. 2 (February 9, 2021): 15. http://dx.doi.org/10.3390/jcdd8020015.

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Proper development and function of the vertebrate heart is vital for embryonic and postnatal life. Many congenital heart defects in humans are associated with disruption of genes that direct the formation or maintenance of atrial and pacemaker cardiomyocytes at the venous pole of the heart. Zebrafish are an outstanding model for studying vertebrate cardiogenesis, due to the conservation of molecular mechanisms underlying early heart development, external development, and ease of genetic manipulation. Here, we discuss early developmental mechanisms that instruct appropriate formation of the venous pole in zebrafish embryos. We primarily focus on signals that determine atrial chamber size and the specialized pacemaker cells of the sinoatrial node through directing proper specification and differentiation, as well as contemporary insights into the plasticity and maintenance of cardiomyocyte identity in embryonic zebrafish hearts. Finally, we integrate how these insights into zebrafish cardiogenesis can serve as models for human atrial defects and arrhythmias.

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27

J. Patterson, A., and L. Zhang. "Hypoxia and Fetal Heart Development." Current Molecular Medicine 10, no. 7 (October 1, 2010): 653–66. http://dx.doi.org/10.2174/156652410792630643.

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28

Smoak, Ida, W. "Hypoglycemia and embryonic heart development." Frontiers in Bioscience 7, no. 1-3 (2002): d307. http://dx.doi.org/10.2741/smoak.

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29

Waardenberg, A. J., M. Ramialison, R. Bouveret, and R. P. Harvey. "Genetic Networks Governing Heart Development." Cold Spring Harbor Perspectives in Medicine 4, no. 11 (October 3, 2014): a013839. http://dx.doi.org/10.1101/cshperspect.a013839.

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30

MARKWALD, ROGER R., COREY H. MJAATVEDT, EDWARD L. KRUG, and ALLAN R. SINNING. "Inductive Interactions in Heart Development." Annals of the New York Academy of Sciences 588, no. 1 Embryonic Ori (April 1990): 13–25. http://dx.doi.org/10.1111/j.1749-6632.1990.tb13193.x.

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31

Olson, E. N., and D. Srivastava. "Molecular Pathways Controlling Heart Development." Science 272, no. 5262 (May 3, 1996): 671–76. http://dx.doi.org/10.1126/science.272.5262.671.

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32

Pickersgill, H. "DEVELOPMENT: Healing a Broken Heart." Science 322, no. 5903 (November 7, 2008): 823a. http://dx.doi.org/10.1126/science.322.5903.823a.

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33

Hurtley, S. M. "Mitochondrial Fusion and Heart Development." Science Signaling 6, no. 301 (November 12, 2013): ec277-ec277. http://dx.doi.org/10.1126/scisignal.2004894.

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34

McFadden, David G., and Eric N. Olson. "Heart development: learning from mistakes." Current Opinion in Genetics & Development 12, no. 3 (June 2002): 328–35. http://dx.doi.org/10.1016/s0959-437x(02)00306-4.

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35

Frisk, M. "Healing heart borrows from development." Science 347, no. 6228 (March 19, 2015): 1325. http://dx.doi.org/10.1126/science.347.6228.1325-n.

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36

Smoak, Ida W. "Hypoglycemia and embryonic heart development." Frontiers in Bioscience 7, no. 4 (2002): d307–318. http://dx.doi.org/10.2741/a776.

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37

Hurtley, S. M. "DEVELOPMENT: Close to the Heart." Science 296, no. 5574 (June 7, 2002): 1769a—1769. http://dx.doi.org/10.1126/science.296.5574.1769a.

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38

Kern, Michael J., Eric A. Argao, and S. Steven Potter. "Homeobox genes and heart development." Trends in Cardiovascular Medicine 5, no. 2 (March 1995): 47–54. http://dx.doi.org/10.1016/1050-1738(94)00033-6.

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39

Santhanakrishnan, Arvind, and Laura A. Miller. "Fluid Dynamics of Heart Development." Cell Biochemistry and Biophysics 61, no. 1 (February 17, 2011): 1–22. http://dx.doi.org/10.1007/s12013-011-9158-8.

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40

Bruneau, Benoit G. "Chromatin remodeling in heart development." Current Opinion in Genetics & Development 20, no. 5 (October 2010): 505–11. http://dx.doi.org/10.1016/j.gde.2010.06.008.

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41

DeBakey, Michael E. "Development of Mechanical Heart Devices." Annals of Thoracic Surgery 79, no. 6 (June 2005): S2228—S2231. http://dx.doi.org/10.1016/j.athoracsur.2005.03.029.

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42

Sylva, Marc, Maurice J. B. van den Hoff, and Antoon F. M. Moorman. "Development of the human heart." American Journal of Medical Genetics Part A 164, no. 6 (April 30, 2013): 1347–71. http://dx.doi.org/10.1002/ajmg.a.35896.

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43

Lockhart, Marie, Elaine Wirrig, Aimee Phelps, and Andy Wessels. "Extracellular matrix and heart development." Birth Defects Research Part A: Clinical and Molecular Teratology 91, no. 6 (May 25, 2011): 535–50. http://dx.doi.org/10.1002/bdra.20810.

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44

Buijtendijk, Marieke F. J., Phil Barnett, and Maurice J. B. Hoff. "Development of the human heart." American Journal of Medical Genetics Part C: Seminars in Medical Genetics 184, no. 1 (February 12, 2020): 7–22. http://dx.doi.org/10.1002/ajmg.c.31778.

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45

Large, Stephen, and Simon Messer. "Machine Perfusion of the Human Heart." Transplantology 3, no. 1 (March 18, 2022): 109–14. http://dx.doi.org/10.3390/transplantology3010011.

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This brief communication about machine perfusion of potential human donor hearts describes its historical development. Included in the review are both the isolated perfusion of donor hearts retrieved from heart beating and non-heart-beating donors. Additionally, some detail of in-situ (within the donor body) normothermic regional reperfusion of the heart and other organs is given. This only applies to the DCD donor heart. Similarly, some detail of ex-situ (outside the body) heart perfusion is offered. This article covers the entire history of the reperfusion of donor hearts. It takes us up to the current day describing 6 years follow-up of these donor machine perfused hearts. These clinical results appear similar to the outcomes of heart beating donors if reperfusion is managed within 30 min of normothermic circulatory determined death. Future developments are also offered. These are 3-fold and include: i. the pressing need for objective markers of the clinical outcome after transplantation, ii. the wish for isolated heart perfusion leading to improvement in donor heart quality, and iii. a strategy to safely lengthen the duration of isolated heart perfusion.

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46

Gunn, J. "Coronary artery stretch versus deep injury in the development of in-stent neointima." Heart 88, no. 4 (October 1, 2002): 401–5. http://dx.doi.org/10.1136/heart.88.4.401.

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47

Bennett, M. R. "IN-STENT STENOSIS: PATHOLOGY AND IMPLICATIONS FOR THE DEVELOPMENT OF DRUG ELUTING STENTS." Heart 89, no. 2 (February 1, 2003): 218–24. http://dx.doi.org/10.1136/heart.89.2.218.

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48

Moorman, A. "DEVELOPMENT OF THE HEART: (1) FORMATION OF THE CARDIAC CHAMBERS AND ARTERIAL TRUNKS." Heart 89, no. 7 (July 1, 2003): 806–14. http://dx.doi.org/10.1136/heart.89.7.806.

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49

Baymetova, Zumradkhon B. "URBAN PLANNING DEVELOPMENT AND HISTORICAL DEVELOPMENT IN ANCIENT CENTRAL ASIA." CURRENT RESEARCH JOURNAL OF HISTORY 02, no. 12 (December 1, 2021): 21–23. http://dx.doi.org/10.37547/history-crjh-02-12-05.

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This article deals with the development of ancient urban planning, its material and spiritual sources, the existence of ancient cultural and material heritage in the heart of our homeland, as well as economic factors in the emergence of cities on the basis of historical facts from primitive society.

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50

Song, Rui, and Lubo Zhang. "Cardiac ECM: Its Epigenetic Regulation and Role in Heart Development and Repair." International Journal of Molecular Sciences 21, no. 22 (November 15, 2020): 8610. http://dx.doi.org/10.3390/ijms21228610.

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The extracellular matrix (ECM) is the non-cellular component in the cardiac microenvironment, and serves essential structural and regulatory roles in establishing and maintaining tissue architecture and cellular function. The patterns of molecular and biochemical ECM alterations in developing and adult hearts depend on the underlying injury type. In addition to exploring how the ECM regulates heart structure and function in heart development and repair, this review conducts an inclusive discussion of recent developments in the role, function, and epigenetic guidelines of the ECM. Moreover, it contributes to the development of new therapeutics for cardiovascular disease.

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Journal articles on the topic 'Heart development'

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