ArticleCells2021
Hepatic Failure in COVID-19: Is Iron Overload the Dangerous Trigger?
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Liver Iron Overload Drives COVID-19 Mortality: a Two-Sample Mendelian Randomization Study.Biological trace element research · 2024Article
- COVID-19 and β-thalassemia: in lieu of evidence and vague nexus.Annals of hematology · 2024Review
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- Iron and iron-related proteins in COVID-19.Clinical and experimental medicine · 2023Review
- COVID-19 induced liver injury from a new perspective: Mitochondria.Mitochondrion · 2023Review
- Digestive system infection by SARS‑CoV‑2: Entry mechanism, clinical symptoms and expression of major receptors (Review).International journal of molecular medicine · 2023Review
- Autopsies Revealed Pathological Features of COVID-19 in Unvaccinated vs. Vaccinated Patients.Biomedicines · 2023Article
- Liver pathology in COVID-19 related death and leading role of autopsy in the pandemic.World journal of gastroenterology · 2023Review
- Liver injury in COVID-19: A minireview.World journal of gastroenterology · 2022Review
- Understanding Long COVID; Mitochondrial Health and Adaptation-Old Pathways, New Problems.Biomedicines · 2022Review
- The sex and gender dimensions of COVID-19: A narrative review of the potential underlying factors.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2022Review
- The spike of SARS-CoV-2 promotes metabolic rewiring in hepatocytes.Communications biology · 2022Article
- COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis.F1000Research · 2022Review
- Metabolic Reprogramming in SARS-CoV-2 Infection Impacts the Outcome of COVID-19 Patients.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Liver injury in COVID-19 patients has progressively emerged, even in those without a history of liver disease, yet the mechanism of liver pathogenicity is still controversial. COVID-19 is frequently associated with increased serum ferritin levels, and hyperferritinemia was shown to correlate with illness severity. The liver is the major site for iron storage, and conditions of iron overload have been established to have a pathogenic role in development of liver diseases. We presented here six patients who developed severe COVID-19, with biochemical evidence of liver failure. Three cases were survived patients, who underwent liver biopsy; the other three were deceased patients, who were autopsied. None of the patients suffered underlying liver pathologies. Histopathological and ultrastructural analyses were performed. The most striking finding we demonstrated in all patients was iron accumulation into hepatocytes, associated with degenerative changes. Abundant ferritin particles were found enclosed in siderosomes, and large aggregates of hemosiderin were found, often in close contact with damaged mitochondria. Iron-caused oxidative stress may be responsible for mitochondria metabolic dysfunction. In agreement with this, association between mitochondria and lipid droplets was also found. Overall, our data suggest that hepatic iron overload could be the pathogenic trigger of liver injury associated to COVID-19.
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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.