ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2020
Coronavirus (Covid-19) sepsis: revisiting mitochondrial dysfunction in pathogenesis, aging, inflammation, and mortality.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
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
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.
- A Review of In Silico Research, SARS-CoV-2, and Neurodegeneration: Focus on Papain-Like Protease.Neurotoxicity research · 2022Pooled it
- Disulfide bond formation between Cys22 and Cys44 in SARS-CoV-2 main protease.Bioorganic & medicinal chemistry letters · 2026Article
- β-Cell Dysfunction in COVID-19 and Post-COVID Syndrome: Molecular Mechanisms Linking Inflammation, Oxidative Stress, and Insulin Secretion.International journal of molecular sciences · 2026Review
- Mitochondria in SARS-CoV-2 infection: Immune interactions and molecular approaches in the Post COVID-19 condition.Genetics and molecular biology · 2026Article
- Analysis of the predictive value of 3-day cumulative energy deficit for 28-day mortality in patients with sepsis and nutritional risk: a retrospective study.Frontiers in nutrition · 2026Article
- Post-COVID-19 syndrome and low-grade inflammation: exploring gender and occupational inequalities in a retrospective cohort study.International health · 2025Article
- Review
- Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.Cell biology and toxicology · 2025Article
- Evaluating the MT-CYB and MT-ATP6 variations in COVID-19 patients: A case-control study.PloS one · 2025Article
- Acute COVID-19 and LongCOVID syndrome - molecular implications for therapeutic strategies - review.Frontiers in immunology · 2025Review
- Identification of diagnostic candidate genes in COVID-19 patients with sepsis.Immunity, inflammation and disease · 2024Article
- Implications of COVID-19 in Parkinson's disease: the purinergic system in a therapeutic-target perspective to diminish neurodegeneration.Purinergic signalling · 2024Review
- Effect of dimethyl fumarate on mitochondrial metabolism in a pediatric porcine model of asphyxia-induced in-hospital cardiac arrest.Scientific reports · 2024Article
- Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID.NPJ science of food · 2024Review
- Amino Acid Metabolism in Leukocytes Showing In Vitro IgG Memory from SARS-CoV2-Infected Patients.Diseases (Basel, Switzerland) · 2024Review
- Association of Inflammatory Mediators with Mitochondrial DNA Variants in Geriatric COVID-19 Patients.Aging and disease · 2024Article
- Sulfide-modified nanoscale zero-valent iron as a novel therapeutic remedy for septic myocardial injury.Journal of advanced research · 2024Article
- The predictive value of peripheral blood cell mitochondrial gene expression in identifying the prognosis in pediatric sepsis at preschool age.Frontiers in cellular and infection microbiology · 2024Article
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- The Potential Role of Nitric Oxide as a Therapeutic Agent against SARS-CoV-2 Infection.International journal of molecular sciences · 2023Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDecline in mitochondrial function occurs with aging and may increase mortality. We discuss mitochondrial contribution to Covid-19 sepsis, specifically the complex interaction of innate immune function, viral replication, hyper-inflammatory state, and HIF-α/Sirtuin pathways.
methodsArticles from PubMed/Medline searches were reviewed using the combination of terms "SARS-CoV-2, Covid-19, sepsis, mitochondria, aging, and immunometabolism".
resultsEvidence indicates that mitochondria in senescent cells may be dysfunctional and unable to keep up with hypermetabolic demands associated with Covid-19 sepsis. Mitochondrial proteins may serve as damage-associated molecular pattern (DAMP) activating innate immunity. Disruption in normal oxidative phosphorylation pathways contributes to elevated ROS which activates sepsis cascade through HIF-α/Sirtuin pathway. Viral-mitochondrial interaction may be necessary for replication and increased viral load. Hypoxia and hyper-inflammatory state contribute to increased mortality associated with Covid-19 sepsis.
conclusionsAging is associated with worse outcomes in sepsis. Modulating Sirtuin activity is emerging as therapeutic agent in sepsis. HIF-α, levels of mitochondrial DNA, and other mitochondrial DAMP molecules may also serve as useful biomarker and need to be investigated. These mechanisms should be explored specifically for Covid-19-related sepsis. Understanding newly discovered regulatory mechanisms may lead to the development of novel diagnostic and therapeutic targets.
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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.