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cardiac fibroblasts

NOTCH1 Is Critical for Fibroblast-Mediated Induction of Cardiomyocyte Specialization Into Ventricular Conduction System-Like Cells In Vitro

[Scientific Reports] Fibroblast-conditioned media (fCM)-mediated response seemed to be spatially-dependent as cardiomyocyte organoids treated with fCM had increased expression of connexin 40 and NAV1.5 primarily on its outer surface.

Infarct Collagen Topography Regulates Fibroblast Fate via p38-Yap-TEAD Signals

[Circulation Research] Adult cardiac fibroblasts were freshly isolated and cultured on ECM topographical mimetics for 72 hours. Aligned mimetics caused cardiac fibroblasts to elongate while randomly organized topographies induced circular morphology similar to the disparate myofibroblast morphologies measured in vivo.

MicroRNA-99b-3p Promotes Angiotensin II-Induced Cardiac Fibrosis in Mice by Targeting GSK-3β

[Acta Pharmacologica Sinica] Upregulation of miR-99b-3p and fibrotic responses were observed in cultured rat cardiac fibroblasts treated with angiotensin II in vitro.

A Specialized Population of Periostin-Expressing Cardiac Fibroblasts Contributes to Postnatal Cardiomyocyte Maturation and Innervation

[Proceedings of the National Academy of Sciences of the United States of America] In order to better understand cardiac fibroblast (CF) functions in heart maturation and postnatal cardiomyocyte cell-cycle arrest, scientists have performed gene expression profiling and ablation of postnatal CF populations.

Acellular Bioscaffolds Redirect Cardiac Fibroblasts and Promote Functional Tissue Repair in Rodents and Humans with Myocardial Injury

[Scientific Reports] Scientists used acellular biologic extracellular matrix scaffolds (bioscaffolds) to stimulate pathways of muscle repair and restore tissue function. They showed that acellular bioscaffolds with bioinductive properties can redirect cardiac fibroblasts to rebuild microvascular networks and avoid tissue fibrosis.

Endothelial-to-Mesenchymal Transition in Anticancer Therapy and Normal Tissue Damage

[Experimental and Molecular Medicine] The authors review the role of hypoxia and reactive oxygen species as the main stimulating factors of tissue damage due to vascular damage and endothelial-to-mesenchymal transition (EndMT). They consider drugs that may be clinically useful for regulating EndMT in various diseases.

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