ArticleCurrent medicinal chemistry2025
Role of Ferroptosis in the Progression of COVID-19 and the Development of Long COVID.
Article in Current medicinal chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Trophoblast ferroptosis restricts SARS-CoV-2 spread in the placenta.bioRxiv : the preprint server for biology · 2026Article
- Aging at the Crossroads of Cuproptosis and Ferroptosis: From Molecular Pathways to Age-Related Pathologies and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Gulf War Illness, Fibromyalgia, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Long COVID Overlap in Common Symptoms and Underlying Biological Mechanisms: Implications for Future Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Ferroptosis and mitochondrial ROS are central to SARS-CoV-2-induced hepatocyte death.Frontiers in cellular and infection microbiology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThis study aimed to examine the role of ferroptosis on the pathogenesis and progression of COVID-19. MATERIALS AND
methodsA total of 127 patients who were hospitalized for COVID-19 were categorized into two groups according to the intensity of oxygen therapy (highflow or low-flow). Clinical characteristics, laboratory parameters, plasma markers, and peripheral blood mononuclear cell (PBMC) markers were measured at baseline and one or two weeks after treatment. Telephone follow-up was performed 3 months after discharge to assess long COVID.
resultsPatients receiving high-flow oxygen therapy had greater levels of neutrophils, D-dimer, C reactive protein, procalcitonin, plasma protein levels of tumor necrosis factor- alpha (TNF-α), interleukin 6 (IL-6), IL-17, acyl-CoA synthetase long-chain family member 4 (ACSL4), and PBMC mRNA level of TNF-α but had lower levels of lymphocytes and plasma glutathione peroxidase 4 (GPX4). There were negative correlations of plasma GPX4 and cystine/glutamate transporter-11 (SLC7A11) with TNF-α, IL-6, and IL-17 and positive correlations of ACSL4 with inflammatory markers in plasma and PBMCs. The plasma levels of TNF-α, IL-6, IL-17, and ACSL4 were significantly lower after treatment than at baseline, but there were higher post-treatment levels of lymphocytes, GPX4, and SLC7A11. Patients with long COVID had a lower baseline level of plasma SLC7A11.
conclusionFerroptosis is activated during the progression of COVID-19, and a low baseline level of a ferroptosis marker (SLC7A11) may indicate an increased risk for long COVID-19. Ferroptosis has potential as a clinical indicator of long COVID and as a therapeutic target.
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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.