ReviewThe journal of venomous animals and toxins including tropical diseases2021
Through DNA sensors and hidden mitochondrial effects of SARS-CoV-2.
Review in The journal of venomous animals and toxins including tropical diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Exaggerated IFN-I Response in Long COVID PBMCs Following Exposure to Viral Mimics.Journal of clinical immunology · 2025Article
- COVID-19 Infection as a Possible Trigger for POLG-Related Mitochondrial Disease: A Case Report.Cureus · 2025Article
- Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024Review
- Review
- Association of Inflammatory Mediators with Mitochondrial DNA Variants in Geriatric COVID-19 Patients.Aging and disease · 2024Article
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- Phase-separated nucleocapsid protein of SARS-CoV-2 suppresses cGAS-DNA recognition by disrupting cGAS-G3BP1 complex.Signal transduction and targeted therapy · 2023Article
- Understanding Long COVID; Mitochondrial Health and Adaptation-Old Pathways, New Problems.Biomedicines · 2022Review
- Melatonin: highlighting its use as a potential treatment for SARS-CoV-2 infection.Cellular and molecular life sciences : CMLS · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The COVID-19 pandemic brought attention to studies about viral infections and their impact on the cell machinery. SARS-CoV-2, for example, invades the host cells by ACE2 interaction and possibly hijacks the mitochondria. To better understand the disease and to propose novel treatments, crucial aspects of SARS-CoV-2 enrolment with host mitochondria must be studied. The replicative process of the virus leads to consequences in mitochondrial function, and cell metabolism. The hijacking of mitochondria, on the other hand, can drive the extrusion of mitochondrial DNA (mtDNA) to the cytosol. Extracellular mtDNA evoke robust proinflammatory responses once detected, that may act in different pathways, eliciting important immune responses. However, few receptors are validated and are able to detect and respond to mtDNA. In this review, we propose that the mtDNA and its detection might be important in the immune process generated by SARS-CoV-2 and that this mechanism might be important in the lung pathogenesis seen in clinical symptoms. Therefore, investigating the mtDNA receptors and their signaling pathways might provide important clues for therapeutic interventions.
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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.