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Persistence of activated myofibroblasts distinguishes non-resolving pathological fibrosis from self-limiting physiological wound healing, indicating that therapies selectively inducing myofibroblast apoptosis could potentially reverse established fibrosis. The acquisition of an apoptosis-resistant phenotype has emerged as a hallmark of scar-forming myofibroblasts during the development and progression of fibrotic diseases. Recent progress in the field has identified molecular pathways promoting survival of activated myofibroblasts, which have unveiled novel therapeutic targets to treat human fibrotic diseases by inducing myofibroblast apoptosis. The so-called B-cell lymphoma 2 homology domain 3 (BH3) mimetic drugs have recently emerged as novel therapeutic agents for reversing established fibrosis in experimental models. This class of drugs unleashes the mitochondrial apoptotic pathway in myofibroblasts by targeting specific anti-apoptotic B-cell lymphoma 2 (BCL-2) proteins.

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