... (CMFs) is considered a critical event in response to the maladaptive cardiac remodeling triggered by angiotensin II (Ang II). Active CMFs are proliferative and contribute to the production of extracellular matrix and matricellular proteins such as periostin, to myocardial fibrosis, and thus to muscle...

... or physiological cardiac hypertrophy, respectively. Although unsettled as far as clinical relevance, numerous studies have linked the Ang II type I (AT 1 ) receptor to adverse cardiac remodeling [ 9 ]. PE also activates a G q/11 -coupled receptor [ 3 ], the cardiac α 1A -adrenergic receptor, which has a protective...

... © 2021 The Author(s). 2021 This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) . aldosterone cardiac remodeling inflammation microRNA-34a TRIF...

... © 2020 The Author(s). 2020 This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) . aldosterone cardiac remodeling inflammation microRNA-34a TRIF...

...-mediated cardiac remodeling. However, the potential mechanisms of aldosterone/inflammatory signaling were still not fully disclosed. The present study aimed to investigate whether TIR-domain-containing adapter-inducing interferon-β (Trif) participated in the aldosterone-induced cardiac remodeling...

... and nuclear translocation in cardiomyocytes. In conclusion, porcupine inhibitor CGX1321 reduces MI injury by limiting fibrosis and promoting regeneration. It promotes cardiomyocyte proliferation by stimulating cell cycle regulating genes with a Hippo/YAP-independent pathway. CGX Cardiac Remodeling...