Key result
MYBPC3 deficiency in cardiac fibroblasts activated NF-κB and TGF-β1 signaling, enhancing aerobic glycolysis and accelerating fibroblast activation to drive hypertrophic cardiomyopathy.
Why the study?
Mutations in MYBPC3 are the most common cause of HCM and myocardial fibrosis is critical to its development, but the mechanism for mutant MYBPC3-induced myocardial fibrosis is not well defined.
MYBPC3 is expressed in cardiac fibroblasts, and its deficiency drives fibroblast activation and myocardial fibrosis via NF-κB/TGF-β1/HIF-1α-mediated metabolic reprogramming, contributing to hypertrophic cardiomyopathy pathogenesis.
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Early MF in MYBPC3-mutant pigs precedes overt HCM; leaves open mechanism and therapeutic targeting in patients.
Zou et al. (2022) studied Hypertrophic cardiomyopathy. MYBPC3 deficiency was evaluated on Cardiac fibroblast activation and myocardial fibrosis. MYBPC3 deficiency in cardiac fibroblasts activated NF-κB and TGF-β1 signaling, enhancing aerobic glycolysis and accelerating fibroblast activation to drive hypertrophic cardiomyopathy.
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