Conditional knockout of IGFBP6 in cardiac fibroblasts and myofibroblasts markedly attenuated post-myocardial infarction fibrotic remodeling, ventricular dysfunction, and isoproterenol-induced cardiac hypertrophy.
Fibroblast-derived IGFBP6 drives cardiac fibrosis via the EGR1-MFAP4 axis, presenting a potential novel therapeutic target for cardiac remodeling disorders.
Our study identifies fibroblast-derived IGFBP6 as a novel regulator of cardiac fibrosis through the EGR1-MFAP4 signaling axis, driving myofibroblasts differentiation and adverse remodeling. Targeting this pathway may offer therapeutic potential for cardiac remodeling disorders.
Cheng et al. (Wed,) conducted a other in Cardiac fibrosis and myocardial infarction (n=56). Cardiac fibroblast and myofibroblast-specific IGFBP6 knockout vs. IGFBP6 f/f (wild-type) mice was evaluated on Cardiac fibrosis, ventricular dysfunction, and infarct size. Conditional knockout of IGFBP6 in cardiac fibroblasts and myofibroblasts markedly attenuated post-myocardial infarction fibrotic remodeling, ventricular dysfunction, and isoproterenol-induced cardiac hypertrophy.