An AIF-mimetic peptide blocked PPIA-mediated AIF-nuclear translocation and reduced both apoptosis and necrosis in embryonic stem cell-derived cardiomyocytes.
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.
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.
Chelko et al. (Wed,) conducted a other in Arrhythmogenic cardiomyopathy. AIF-mimetic peptide was evaluated on Apoptosis and necrosis. An AIF-mimetic peptide blocked PPIA-mediated AIF-nuclear translocation and reduced both apoptosis and necrosis in embryonic stem cell-derived cardiomyocytes.
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