Langendorff system was applied to isolate cardiomyocytes and cardiac fibroblasts from transverse aortic constriction-induced mice.
[Signal Transduction and Targeted Therapy]
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Zhang, X., Yuan, S., Li, H., Zhan, J., Wang, F., Fan, J., Nie, X., Wang, Y., Wen, Z., Chen, Y., Chen, C., & Wang, D. W. (2021). The double face of miR-320: cardiomyocytes-derived miR-320 deteriorated while fibroblasts-derived miR-320 protected against heart failure induced by transverse aortic constriction. Signal Transduction and Targeted Therapy, 6(1), 1–12. https://doi.org/10.1038/s41392-020-00445-8 Cite
Researchers demonstrated using adult cardiac fibroblasts that genetic deletion of G protein-coupled receptor kinase 5 inhibits angiotensin II-mediated fibroblast activation.
[Proceedings of the National Academy of Sciences of the United States of America]
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5-HT2B antagonism resulted in collagen fiber redistribution to thinner collagen fibers which were more anisotropic, enhancing left ventricular contractility, while fibrotic tissue stiffness was decreased, limiting the hypertrophic response of uninjured cardiomyocytes.
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Snider J. Caleb, Riley Lance A., Mallory Noah T., Bersi Matthew R., Umbarkar Prachi, Gautam Rekha, Zhang Qinkun, Mahadevan-Jansen Anita, Hatzopoulos Antonis K., Maroteaux Luc, Lal Hind, & Merryman W. David. (n.d.). Targeting 5-HT2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling after Myocardial Infarction. Circulation, 0(0). https://doi.org/10.1161/CIRCULATIONAHA.120.051517 Cite
Among the 32 neutrophil gelatinase-associated lipocalin (NGAL) inhibitors tested, GPZ614741 and GPZ058225 fully blocked NGAL-induced inflammatory and profibrotic markers in human cardiac fibroblasts and primary mouse kidney fibroblasts.
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Antifibrotic effect of novel neutrophil gelatinase-associated lipocalin inhibitors in cardiac and renal disease models | Scientific Reports. (n.d.). Retrieved January 28, 2021, from https://www.nature.com/articles/s41598-021-82279-0 Cite
Scientists summarize the latest research progress in cardiac regeneration and heart repair through altering cardiomyocyte fate plasticity, which is emerging as an effective strategy to compensate for the loss of functional cardiomyocytes and improve the impaired heart functions.
[Signal Transduction and Targeted Therapy]
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Neonatal rat cardiomyocytes and cardiac fibroblasts were used to validate the protective effects of 6-gingerol in response to phenylephrine and transforming growth factor-β challenge.
[Acta Pharmacologica Sinica]
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Mechanistic studies revealed roles of eosinophil IL4 and cationic protein mEar1 in blocking H2O2– and hypoxia-induced mouse and human cardiomyocyte death, TGF-β-induced cardiac fibroblast Smad2/3 activation, and TNF-α-induced neutrophil adhesion on the heart endothelial cell monolayer.
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The role of cardiac IgE receptor (FcεR1) signaling in pathological cardiac remodeling was explored in vivo by FcεR1 genetic depletion, anti-IgE antibodies, and bone-marrow transplantation. The roles of immunoglobulin E (IgE)-FcεR1 pathway were further evaluated in vitro in primary cultured rat cardiomyocytes and cardiac fibroblasts.
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β-adrenergic receptor (β-AR) overactivation induced inflammasome activation in both the cardiomyocytes and cardiac fibroblasts of mice hearts following a subcutaneous injection of isoproterenol, a selective agonist of β-AR.
[Cell Death & Disease]
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In rat and mouse models of ischemic heart failure, investigators showed that miR-30d gain of function improves cardiac function, decreases myocardial fibrosis, and attenuates cardiomyocyte apoptosis.
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The authors briefly survey cell sources and delivery strategies, along with biomaterials and their processing techniques, developed for myocardial infarction treatment. Key issues and challenges, as well as recommendations for future research, are also discussed.
[Advanced Healthcare Materials]
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