ReviewAntioxidants (Basel, Switzerland)2021
Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 65 citations in OpenAlex.
- Mitochondria as integrative regulators of ferroptosis in the female reproductive system.Biology of reproduction · 2026Review
- Clinical implications of ferroptosis in critical illness: a narrative review.Journal of intensive care · 2026Review
- Impact of COVID-19 Booster Vaccination on Serum Redox Homeostasis.International journal of molecular sciences · 2026Article
- Plasma Membrane Redox Failure Links COVID-19 Metabolic Stress to Ferroptotic Neurodegeneration.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondria-driven ferroptosis in intervertebral disc degeneration: A novel target in age-related spinal diseases (Review).Experimental and therapeutic medicine · 2026Review
- SARS-CoV-2 Spike Protein Induces Time-Dependent and Brain-Region-Specific Alterations in Ferroptosis Markers: A Preliminary Study in K18-hACE2 Mice.International journal of molecular sciences · 2026Article
- Ferroptosis-associated genes as candidate biomarkers for the identification of patients with severe influenza necessitating mechanical ventilation.BMJ open respiratory research · 2025Article
- Ferroptosis and Metabolic Dysregulation: Emerging Chemical Targets in Cancer and Infection.Molecules (Basel, Switzerland) · 2025Review
- Metabolic Reprogramming in Respiratory Viral Infections: A Focus on SARS-CoV-2, Influenza, and Respiratory Syncytial Virus.Biomolecules · 2025Review
- Iron and ferroptosis in kidney disease: molecular and metabolic mechanisms.Frontiers in immunology · 2025Review
- Ferroptosis and mitochondrial ROS are central to SARS-CoV-2-induced hepatocyte death.Frontiers in cellular and infection microbiology · 2025Article
- Cathepsin B induces kidney diseases through different types of programmed cell death.Frontiers in immunology · 2025Review
- Visual analysis on ferroptosis and its cross-talk to coronavirus disease 2019 (COVID-19).Heliyon · 2024Article
- Review
- Mechanisms and therapeutic targets of ferroptosis: Implications for nanomedicine design.Journal of pharmaceutical analysis · 2024Review
- Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration.Molecular neurodegeneration · 2024Review
- Alterations in microbiota of patients with COVID-19: implications for therapeutic interventions.MedComm · 2024Review
- Human transferrin receptor can mediate SARS-CoV-2 infection.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- COVID-19, Possible Hepatic Pathways and Alcohol Abuse-What Do We Know up to 2023?International journal of molecular sciences · 2024Review
- SARS-CoV-2 Accessory Protein Orf7b Induces Lung Injury via c-Myc Mediated Apoptosis and Ferroptosis.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent programmed cell death. The term ferroptosis was coined in the last decade to describe the form of cell death induced by the small molecule erastin. As a specific inducer of ferroptosis, erastin inhibits cystine-glutamate antiporter system Xc-, blocking transportation into the cytoplasm of cystine, a precursor of glutathione (GSH) in exchange with glutamate and the consequent malfunction of GPX4. Ferroptosis is also promoted by intracellular iron overload and by the iron-dependent accumulation of polyunsaturated fatty acids (PUFA)-derived lipid peroxides. Since depletion of GSH, inactivation of GPX4, altered iron metabolism, and upregulation of PUFA peroxidation by reactive oxygen species are peculiar signs of COVID-19, there is the possibility that SARS-CoV-2 may trigger ferroptosis in the cells of multiple organs, thus contributing to multiorgan damage. Here, we review the molecular mechanisms of ferroptosis and its possible relationship with SARS-CoV-2 infection and multiorgan damage. Finally, we analyze the potential interventions that may combat ferroptosis and, therefore, reduce multiorgan damage.
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