Observational studyHistology and histopathology2021
The kidnapping of mitochondrial function associated with the SARS-CoV-2 infection.
Observational study in Histology and histopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.Cell biology and toxicology · 2025Article
- The protein interaction of mitochondrial transcription factors A and B2 is associated with 30-day survival in critical COVID-19.Frontiers in immunology · 2025Article
- Mitochondrial dysfunction in acute and post-acute phases of COVID-19 and risk of non-communicable diseases.npj metabolic health and disease · 2024Review
- Redox Homeostasis Alteration Is Restored through Melatonin Treatment in COVID-19 Patients: A Preliminary Study.International journal of molecular sciences · 2024Article
- Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID.NPJ science of food · 2024Review
- New Insights into the Effects of SARS-CoV-2 on Metabolic Organs: A Narrative Review of COVID-19 Induced Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Connecting dots of long COVID-19 pathogenesis: a vagus nerve- hypothalamic-pituitary- adrenal-mitochondrial axis dysfunction.Frontiers in cellular and infection microbiology · 2024Review
- Selenium-More than Just a Fortuitous Sulfur Substitute in Redox Biology.Molecules (Basel, Switzerland) · 2023Review
- Pathophysiological involvement of host mitochondria in SARS-CoV-2 infection that causes COVID-19: a comprehensive evidential insight.Molecular and cellular biochemistry · 2023Review
- Possible Pathogenesis and Prevention of Long COVID: SARS-CoV-2-Induced Mitochondrial Disorder.International journal of molecular sciences · 2023Review
- N-Acetyl Cysteine Restores the Diminished Activity of the Antioxidant Enzymatic System Caused by SARS-CoV-2 Infection: Preliminary Findings.Pharmaceuticals (Basel, Switzerland) · 2023Article
- PPAR Alpha Activation by Clofibrate Alleviates Ischemia/Reperfusion Injury in Metabolic Syndrome Rats by Decreasing Cardiac Inflammation and Remodeling and by Regulating the Atrial Natriuretic Peptide Compensatory Response.International journal of molecular sciences · 2023Article
- Molecular Mechanisms Related to Responses to Oxidative Stress and Antioxidative Therapies in COVID-19: A Systematic Review.Antioxidants (Basel, Switzerland) · 2022Review
- Targeting the YXXΦ Motifs of the SARS Coronaviruses 1 and 2 ORF3a Peptides by In Silico Analysis to Predict Novel Virus-Host Interactions.Biomolecules · 2022Article
- [Evolutionary cardiology and experimental research].Archivos de cardiologia de Mexico · 2022Article
- Article
- Effect of Hyperglycemia on COVID-19 Outcomes: Vaccination Efficacy, Disease Severity, and Molecular Mechanisms.Journal of clinical medicine · 2022Review
- Article
- COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis.F1000Research · 2022Review
- Imaging Techniques: Essential Tools for the Study of SARS-CoV-2 Infection.Frontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) leads to multi-organ failure associated with a cytokine storm and septic shock. The virus evades the mitochondrial production of interferons through its N protein and, from that moment on, it hijacks the functions of these organelles. The aim of this study was to show how the virus kidnaps the mitochondrial machinery for its benefit and survival, leading to alterations of serum parameters and to nitrosative stress (NSS). In a prospective cohort of 15 postmortem patients who died from COVID-19, six markers of mitochondrial function (COX II, COX IV, MnSOD, nitrotyrosine, Bcl-2 and caspase-9) were analyzed by the immune colloidal gold technique in samples from the lung, heart, and liver. Biometric laboratory results from these patients showed alterations in hemoglobin, platelets, creatinine, urea nitrogen, glucose, C-reactive protein, albumin, D-dimer, ferritin, fibrinogen, Ca²⁺, K⁺, lactate and troponin. These changes were associated with alterations in the mitochondrial structure and function. The multi-organ dysfunction present in COVID-19 patients may be caused, in part, by damage to the mitochondria that results in an inflammatory state that contributes to NSS, which activates the sepsis cascade and results in increased mortality in COVID-19 patients.
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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.