ReviewMolecular neurobiology2021
Neurological Implications of COVID-19: Role of Redox Imbalance and Mitochondrial Dysfunction.
Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The trial behind it
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Dose assessment of melatonin in sepsis (DAMSEL2) study: Pharmacokinetics of two doses of oral melatonin in patients with sepsis.Journal of pineal research · 2022Trial
- Mitochondrial Reactive Oxygen Species: A Unifying Mechanism in Long COVID and Spike Protein-Associated Injury: A Narrative Review.Biomolecules · 2025Review
- Does COVID-19 Trigger the Risk for the Development of Parkinson's Disease? Therapeutic Potential of Vitamin C.Molecular neurobiology · 2024Review
- Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID.NPJ science of food · 2024Review
- Understanding Post-COVID-19: Mechanisms, Neurological Complications, Current Treatments, and Emerging Therapies.International journal of general medicine · 2024Article
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- Immune landscape and redox imbalance during neurological disorders in COVID-19.Cell death & disease · 2023Review
- Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies.Acta pharmacologica Sinica · 2023Review
- COVID-19 metabolism: Mechanisms and therapeutic targets.MedComm · 2022Review
- Mitochondrial hijacking: A potential mechanism for SARS-CoV-2 to impair female fertility.Medical hypotheses · 2022Article
- COVID-19 pandemic: A multidisciplinary perspective on the pathogenesis of a novel coronavirus from infection, immunity and pathological responses.Frontiers in immunology · 2022Review
- Can SARS-CoV-2 Infection Lead to Neurodegeneration and Parkinson's Disease?Brain sciences · 2021Review
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 at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 or COVID-19 has been declared as a pandemic disease by the World Health Organization (WHO). Globally, this disease affected 159 million of the population and reported ~ 3.3 million deaths to the current date (May 2021). There is no definitive treatment strategy that has been identified, although this disease has prevailed in its current form for the past 18 months. The main challenges in the (SARS-CoV)-2 infections are in identifying the heterogeneity in viral strains and the plausible mechanisms of viral infection to human tissues. In parallel to the investigations into the patho-mechanism of SARS-CoV-2 infection, understanding the fundamental processes underlying the clinical manifestations of COVID-19 is very crucial for designing effective therapies. Since neurological symptoms are very apparent in COVID-19 infected patients, here, we tried to emphasize the involvement of redox imbalance and subsequent mitochondrial dysfunction in the progression of the COVID-19 infection. It has been articulated that mitochondrial dysfunction is very apparent and also interlinked to neurological symptoms in COVID-19 infection. Overall, this article provides an in-depth overview of redox imbalance and mitochondrial dysfunction involvement in aggravating COVID-19 infection and its probable contribution to the neurological manifestation of the disease.
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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.