Abstract Fri126: Mitochondrial Proteostasis In Cardiac Fibroblast Activation And Fibrosis

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CLPB loss leads to pro-fibrotic changes in cardiac fibroblasts and disrupts metabolic balance.
CLPB expression is reduced in activated fibroblasts exposed to TGFβ and Ang II, with significant implications.
Cardiac spheroid models highlight that absence of CLPB results in contractile dysfunction, worsening heart conditions.
Targeting CLPB may offer new strategies for managing cardiac fibrosis and related heart failure.

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Observational analysis shows that CLPB regulates fibrosis and mitochondrial function in cardiac fibroblasts, indicating its therapeutic potential.

Goyani et al. (2025) studied this question.

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Observational analysis shows that CLPB regulates fibrosis and mitochondrial function in cardiac fibroblasts, indicating its therapeutic potential.