Key result
Inhibition of calpain activity attenuated coxsackievirus B3-induced myocarditis by reducing mitochondrial fission and cardiomyocyte apoptosis.
Why the study?
Elevated calpain activity was known to be involved in the pathogenesis of viral myocarditis, but the underlying mechanisms required further exploration.
Does calpain inhibition reduce cardiomyocyte apoptosis and mitochondrial fission in a preclinical model of acute viral myocarditis?
Does calpain inhibition reduce cardiomyocyte apoptosis and mitochondrial fission in a preclinical model of acute viral myocarditis?
p-value: p=<0.05
Calpain inhibition protects against CVB3-induced viral myocarditis by suppressing Drp-1-mediated mitochondrial fission and subsequent cardiomyocyte apoptosis.
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Calpain inhibition may attenuate apoptosis in VMC models; leaves open whether targeting calpain improves outcomes in human viral myocarditis.
Shi et al. (2021) studied Acute viral myocarditis (n=32). Calpain inhibition (calpastatin overexpression or PD150606) vs. Wild-type or vehicle control was evaluated on Cardiomyocyte apoptosis and mitochondrial fission (p=<0.05). Inhibition of calpain activity attenuated coxsackievirus B3-induced myocarditis by reducing mitochondrial fission and cardiomyocyte apoptosis.
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