Remdesivir induces persistent mitochondrial and structural damage in human induced pluripotent stem cell-derived cardiomyocytes
et al., Cardiovascular Research, doi:10.1093/cvr/cvab311, Oct 2021
In vitro study showing that remdesivir induces persistent cardiotoxicity in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) at clinically relevant concentrations. Authors exposed hiPSC-CMs to remdesivir (0.1-12.5 μM) under normoxic and hypoxic conditions and found dose-dependent mitochondrial dysfunction, including fragmentation, reduced redox potential, and suppressed respiration at concentrations as low as 2.5 μM (below the estimated plasma concentration). Non-mitochondrial damage including electrophysiological alterations and sarcomere disarray were also observed. These changes persisted after cessation of treatment and culminated in increased cell death.
Gérard, Zhou, Wu, Kamo, Choi, Kim show increased risk of acute kidney injury, Leo, Briciu, Muntean, Petrov show increased risk of liver injury, and Negru, Cheng, Mohammed, Kwok show increased risk of cardiac disorders with remdesivir.
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Kwok et al., 5 Oct 2021, China, peer-reviewed, 10 authors.
Contact: ellen.poon@cuhk.edu.hk.
In vitro studies are an important part of preclinical research, however results may be very different in vivo.
Remdesivir induces persistent mitochondrial and structural damage in human induced pluripotent stem cell-derived cardiomyocytes
Cardiovascular Research, doi:10.1093/cvr/cvab311
Aims Remdesivir is a prodrug of an adenosine triphosphate analogue and is currently the only drug formally approved for the treatment of hospitalized coronavirus disease of 2019 (COVID-19) patients. Nucleoside/nucleotide analogues have been shown to induce mitochondrial damage and cardiotoxicity, and this may be exacerbated by hypoxia, which frequently occurs in severe COVID-19 patients. Although there have been few reports of adverse cardiovascular events associated with remdesivir, clinical data are limited. Here, we investigated whether remdesivir induced cardiotoxicity using an in vitro human cardiac model. .......
Supplementary material Supplementary material is available at Cardiovascular Research online.
Authors' contributions
References
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DOI record:
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"abstract": "<jats:title>Abstract</jats:title>\n <jats:sec>\n <jats:title>Aims</jats:title>\n <jats:p>Remdesivir is a prodrug of an adenosine triphosphate analogue and is currently the only drug formally approved for the treatment of hospitalized coronavirus disease of 2019 (COVID-19) patients. Nucleoside/nucleotide analogues have been shown to induce mitochondrial damage and cardiotoxicity, and this may be exacerbated by hypoxia, which frequently occurs in severe COVID-19 patients. Although there have been few reports of adverse cardiovascular events associated with remdesivir, clinical data are limited. Here, we investigated whether remdesivir induced cardiotoxicity using an in vitro human cardiac model.</jats:p>\n </jats:sec>\n <jats:sec>\n <jats:title>Methods and results</jats:title>\n <jats:p>Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were exposed to remdesivir under normoxic and hypoxic conditions to simulate mild and severe COVID-19, respectively. Remdesivir induced mitochondrial fragmentation, reduced redox potential, and suppressed mitochondrial respiration at levels below the estimated plasma concentration under both normoxic and hypoxic conditions. Non-mitochondrial damage such as electrophysiological alterations and sarcomere disarray were also observed. Importantly, some of these changes persisted after the cessation of treatment, culminating in increased cell death. Mechanistically, we found that inhibition of DRP1, a regulator of mitochondrial fission, ameliorated the cardiotoxic effects of remdesivir, showing that remdesivir-induced cardiotoxicity was preventable and excessive mitochondrial fission might contribute to this phenotype.</jats:p>\n </jats:sec>\n <jats:sec>\n <jats:title>Conclusions</jats:title>\n <jats:p>Using an in vitro model, we demonstrated that remdesivir can induce cardiotoxicity in hiPSC-CMs at clinically relevant concentrations. These results reveal previously unknown potential side-effects of remdesivir and highlight the importance of further investigations with in vivo animal models and active clinical monitoring to prevent lasting cardiac damage to patients.</jats:p>\n </jats:sec>",
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