ReviewMolecular and cellular biochemistry2023
Pathophysiological involvement of host mitochondria in SARS-CoV-2 infection that causes COVID-19: a comprehensive evidential insight.
Review in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 67 citations in OpenAlex.
- SARS-CoV-2 envelope protein mitochondrial localization reveals host metabolic disruption.The Journal of biological chemistry · 2026Article
- The Post-COVID syndrome caused by excessive inflammation: pathogenesis, potential targets and therapeutic agents.Frontiers in pharmacology · 2026Review
- Multi-omics Analysis Implicates Mitochondrial Complex Assembly Protein COX18 in Mitochondrial Signaling and Tumorigenesis across Cancers.Cell biochemistry and biophysics · 2025Article
- Severe myocardium suppression in two congenital heart disease patients after remdesivir use - a case report.BMC pediatrics · 2025Article
- Mechanisms of Mitochondrial Impairment by SARS-CoV-2 Proteins: A Nexus of Pathogenesis with Significant Biochemical and Clinical Implications.International journal of molecular sciences · 2025Review
- Article
- Mitochondrial Reactive Oxygen Species: A Unifying Mechanism in Long COVID and Spike Protein-Associated Injury: A Narrative Review.Biomolecules · 2025Review
- Novel biomarkers of mitochondrial dysfunction in Long COVID patients.GeroScience · 2025Article
- mTORC1 syndrome (TorS): unifying paradigm for PASC, ME/CFS and PAIS.Journal of translational medicine · 2025Review
- Mitochondria and the Repurposing of Diabetes Drugs for Off-Label Health Benefits.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
- Porcine Epidemic Diarrhea Virus Infection of Porcine Intestinal Epithelial Cells Causes Mitochondrial DNA Release and the Activation of the NLRP3 Inflammasome to Mediate Interleukin-1β Secretion.Veterinary sciences · 2024Article
- HbA1c and leukocyte mtDNA levels as major factors associated with post-COVID-19 syndrome in type 2 diabetes patients.Scientific reports · 2024Article
- Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches.GeroScience · 2024Review
- Nanobody against SARS-CoV-2 non-structural protein Nsp9 inhibits viral replication in human airway epithelia.Molecular therapy. Nucleic acids · 2024Article
- Cyclosporin A as an Add-On Therapy to a Corticosteroid-Based Background Treatment in Patients with COVID-19: A Multicenter, Randomized Clinical Trial.Journal of clinical medicine · 2024Article
- Dynamic label-free analysis of SARS-CoV-2 infection reveals virus-induced subcellular remodeling.Nature communications · 2024Article
- The metabolic footprint of Vero E6 cells highlights the key metabolic routes associated with SARS-CoV-2 infection and response to drug combinations.Scientific reports · 2024Article
- Article
- Decoding HiPSC-CM's Response to SARS-CoV-2: mapping the molecular landscape of cardiac injury.BMC genomics · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
SARS-CoV-2 is a positive-strand RNA virus that infects humans through the nasopharyngeal and oral route causing COVID-19. Scientists left no stone unturned to explore a targetable key player in COVID-19 pathogenesis against which therapeutic interventions can be initiated. This article has attempted to review, coordinate and accumulate the most recent observations in support of the hypothesis predicting the altered state of mitochondria concerning mitochondrial redox homeostasis, inflammatory regulations, morphology, bioenergetics and antiviral signalling in SARS-CoV-2 infection. Mitochondria is extremely susceptible to physiological as well as pathological stimuli, including viral infections. Recent studies suggest that SARS-CoV-2 pathogeneses alter mitochondrial integrity, in turn mitochondria modulate cellular response against the infection. SARS-CoV-2 M protein inhibited mitochondrial antiviral signalling (MAVS) protein aggregation in turn hinders innate antiviral response. Viral open reading frames (ORFs) also play an instrumental role in altering mitochondrial regulation of immune response. Notably, ORF-9b and ORF-6 impair MAVS activation. In aged persons, the NLRP3 inflammasome is over-activated due to impaired mitochondrial function, increased mitochondrial reactive oxygen species (mtROS), and/or circulating free mitochondrial DNA, resulting in a hyper-response of classically activated macrophages. This article also tries to understand how mitochondrial fission-fusion dynamics is affected by the virus. This review comprehends the overall mitochondrial attribute in pathogenesis as well as prognosis in patients infected with COVID-19 taking into account pertinent in vitro, pre-clinical and clinical data encompassing subjects with a broad range of severity and morbidity. This endeavour may help in exploring novel non-canonical therapeutic strategies to COVID-19 disease and associated complications.
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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.