Preventing CAPN1-induced AIF-truncation or barring binding of AIF to PPIA may avert myocyte death and disease progression to heart failure in arrhythmogenic cardiomyopathy.
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Hypothesis-generating for AIF-PPIA targeting in arrhythmogenic cardiomyopathy; requires in vivo and clinical validation before any therapeutic consideration.
ES-CMs with an AIF-mimetic peptide, mirroring the cyclophilin-A (PPIA) binding site of AIF, blocked PPIA-mediated AIF-nuclear translocation, and reduced both apoptosis and necrosis. Thus, preventing CAPN1-induced AIF-truncation or barring binding of AIF to the nuclear chaperone, PPIA, may avert myocyte death and, ultimately, disease progression to heart failure in ACM and likely other forms of cardiomyopathies.
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Chelko et al. (2021) studied Arrhythmogenic cardiomyopathy. AIF-mimetic peptide was evaluated on Apoptosis and necrosis.
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