ArticleToxicology and applied pharmacology2021
Remdesivir; molecular and functional measures of mitochondrial safety.
Article in Toxicology and applied pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Remdesivir nephrotoxicity in tubular epithelial cells.Frontiers in pharmacology · 2026Article
- Severe myocardium suppression in two congenital heart disease patients after remdesivir use - a case report.BMC pediatrics · 2025Article
- Selective Inhibition of Vascular Smooth Muscle Cell Function by COVID-19 Antiviral Drugs: Impact of Heme Oxygenase-1.Antioxidants (Basel, Switzerland) · 2025Article
- Presentation of vitiligo in a case of COVID-19 infection concomitant with receiving remdesivir.Clinical case reports · 2024Article
- Remdesivir Discontinuation Decisions Based on Thresholds of Aminotransferase in an Observational Registry.Drugs · 2024Article
- Transient Lactic Acidosis and Elevation of Transaminases after the Introduction of Remdesivir in a Patient with Acute Kidney Injury.Case reports in critical care · 2024Article
- Electrophysiological and sick sinus syndrome effects of Remdesivir challenge in guinea-pig hearts.Frontiers in physiology · 2024Article
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- Adverse Events in Pregnant Patients Treated with Coronavirus Disease 2019 Therapeutics.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2023Article
- Remdesivir increases mtDNA copy number causing mild alterations to oxidative phosphorylation.Scientific reports · 2023Article
- Recent Advances in Molecular Mechanisms of Nucleoside Antivirals.Current issues in molecular biology · 2023Review
- COVID-19 induced liver injury from a new perspective: Mitochondria.Mitochondrion · 2023Review
- Long COVID-19 and the Heart: Is Cardiac Mitochondria the Missing Link?Antioxidants & redox signaling · 2023Review
- Developmental toxicity of remdesivir, an anti-COVID-19 drug, is implicated by in vitro assays using morphogenetic embryoid bodies of mouse and human pluripotent stem cells.Birth defects research · 2023Article
- Inhibition of Viral RNA-Dependent RNA Polymerases by Nucleoside Inhibitors: An Illustration of the Unity and Diversity of Mechanisms.International journal of molecular sciences · 2022Review
- Remdesivir impairs mouse preimplantation embryo development at therapeutic concentrations.Reproductive toxicology (Elmsford, N.Y.) · 2022Article
- Molnupiravir; molecular and functional descriptors of mitochondrial safety.Toxicology and applied pharmacology · 2022Article
- Remdesivir does not affect mitochondrial DNA copy number or deletion mutation frequency in aged male rats: A short report.PloS one · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Remdesivir is one of a few antiviral drugs approved for treating severe cases of coronavirus 2 (SARS-CoV-2) infection in hospitalized patients. The prodrug is a nucleoside analog that interferes with viral replication by inhibiting viral RNA-dependent RNA polymerase. The drug has also been shown to be a weak inhibitor of human mitochondrial RNA polymerase, leaving open the possibility of mitochondrial off-targets and toxicity. The investigation was designed to explore whether remdesivir causes mitochondrial toxicity, using both genomic and functional parameters in the assessment. Human-derived HepG2 liver cells were exposed for up to 48 h in culture to increasing concentrations of remdesivir. At sub-cytotoxic concentrations (<1 μM), the drug failed to alter either the number of copies or the expression of the mitochondrial genome. mtDNA copy number was unaffected as was the relative rates of expression of mtDNA-encoded and nuclear encoded subunits of complexes I and IV of the mitochondrial respiratory chain. Consistent with this is the observation that remdesivir was without effect on mitochondrial respiration, including basal respiration, proton leak, maximum uncoupled respiration, spare respiratory capacity or coupling efficiency. We conclude that although remdesivir has weak inhibitory activity towards mitochondrial RNA polymerase, mitochondria are not primary off-targets for the mechanism of cytotoxicity of the drug.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.