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cardiac fibroblasts

HDAC Inhibition Reverses Preexisting Diastolic Dysfunction and Blocks Covert Extracellular Matrix Remodeling

[Circulation] Researchers addressed the therapeutic potential of histone deacetylases (HDAC) inhibition in a model of established diastolic dysfunction with preserved ejection fraction.

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] Langendorff system was applied to isolate cardiomyocytes and cardiac fibroblasts from transverse aortic constriction-induced mice.

GRK5 Is a Regulator of Fibroblast Activation and Cardiac Fibrosis

[Proceedings of the National Academy of Sciences of the United States of America] Researchers demonstrated using adult cardiac fibroblasts that genetic deletion of G protein-coupled receptor kinase 5 inhibits angiotensin II-mediated fibroblast activation.

Targeting 5-HT2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling after Myocardial Infarction

[Circulation] 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.

Antifibrotic Effect of Novel Neutrophil Gelatinase-Associated Lipocalin Inhibitors in Cardiac and Renal Disease Models

[Scientific Reports] 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.

Regulation of Cardiomyocyte Fate Plasticity: A Key Strategy for Cardiac Regeneration

[Signal Transduction and Targeted Therapy] 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.

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