Reports suggest that the Middle East respiratory syndrome-related coronavirus (MERS-CoV) can cause acute myocarditis and heart failure. SARS-CoV-2 and MERS-CoV have similar pathogenicity, and the myocardial damage caused by infection with these viruses undoubtedly increases the difficulty and complexity of patient treatment. Myocardial injury associated with the SARS-CoV-2 occurred in 5 of the first 41 patients diagnosed with COVID-19 in Wuhan

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Impaired mitochondrial ATP production in cardiomyocytes is one of the major causes of heart failure. A drug that maintains ATP production would, therefore, be an attractive heart failure treatment option.

We performed high-throughput image-based screens under hypoxia, and identified mitochondrial ATP protectors, including the anti-parasite drug, ivermectin. We show that ivermectin increased mitochondrial ATP production by inducing Cox6a2 expression and inhibited the hypertrophic response of human iPSC-derived cardiomyocytes. Pharmacological inhibition of importin ß, a target of ivermectin, exhibited similar protective effects.

Our studies indicate that compounds maintaining mitochondrial ATP under hypoxia may prevent pathological hypertrophy and improve cardiac function.

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