Key result
CLPB loss promotes cardiac fibroblast activation, glycolytic metabolic reprogramming, and contractile dysfunction under fibrotic stress.
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Loss of the mitochondrial chaperonin CLPB promotes a pro-fibrotic phenotype and metabolic reprogramming in cardiac fibroblasts, suggesting it as a potential therapeutic target for cardiac fibrosis.
Goyani et al. (2025) studied Cardiac fibrosis. CLPB deficiency vs. Wild-type was evaluated on Fibroblast activation, metabolic reprogramming, and contractile dysfunction. Loss of CLPB in cardiac fibroblasts led to a pro-fibrotic phenotype, metabolic reprogramming toward glycolysis, and contractile dysfunction in response to fibrotic stimuli.
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