Distinct phenotypes induced by acute hypoxia and TGF-β1 in human adult cardiac fibroblasts.

ABSTRACT: Myocardial infarction (MI) causes hypoxic injury to downstream myocardial tissue, which initiates a wound healing response that replaces injured myocardial tissue with a scar. Wound healing is a complex process that consists of multiple phases, in which many different stimuli induce cardiac fibroblasts to differentiate into myofibroblasts and deposit new matrix. While this process is necessary to replace necrotic tissue, excessive and unresolved fibrosis is common post-MI and correlated with heart failure. Therefore, defining how cardiac fibroblast phenotypes are distinctly regulated by stimuli that are prevalent in the post-MI microenvironment, such as hypoxia and transforming growth factor-beta (TGF-β), is essential for understanding and ultimately mitigating pathological fibrosis. In th

SUBMITTER: Khalil NN 

PROVIDER: S-EPMC11423773 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature