Population
Preclinical models of cardiac remodeling (specifics not detailed in abstract)
Design
Preclinical
Key result
Conditional knockout of IGFBP6 in cardiac fibroblasts and myofibroblasts markedly attenuated post-myocardial infarction fibrotic remodeling, ventricular dysfunction, and isoproterenol-induced cardiac hypertrophy.
Authors
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Does not support clinical targeting yet; leaves open validation of this axis in human cardiac remodeling trials.
Fibroblast-derived IGFBP6 drives cardiac fibrosis via the EGR1-MFAP4 axis, presenting a potential novel therapeutic target for cardiac remodeling disorders.
Cheng et al. (2025) studied 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.