ArticleACS chemical neuroscience2022
Mitochondrial Dysfunction: A Prelude to Neuropathogenesis of SARS-CoV-2.
Article in ACS chemical neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Direct RNA sequencing reveals m6A modifications and isoform changes in SARS-CoV-2-infected HEK cells.Access microbiology · 2025Article
- Assessment of Placental Antioxidant Defense Markers in Vaccinated and Unvaccinated COVID-19 Third-Trimester Pregnancies.Life (Basel, Switzerland) · 2024Article
- Focusing on mitochondria in the brain: from biology to therapeutics.Translational neurodegeneration · 2024Review
- Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID.NPJ science of food · 2024Review
- Investigating the Potential Shared Molecular Mechanisms between COVID-19 and Alzheimer's Disease via Transcriptomic Analysis.Viruses · 2024Article
- The effects of urolithin A on poly I:C-induced microglial activation.Frontiers in cellular neuroscience · 2024Article
- Aging mitochondria in the context of SARS-CoV-2: exploring interactions and implications.Frontiers in aging · 2024Review
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- Human-derived air-liquid interface cultures decipher Alzheimer's disease-SARS-CoV-2 crosstalk in the olfactory mucosa.Journal of neuroinflammation · 2023Article
- The Ways of the Virus: Interactions of Platelets and Red Blood Cells with SARS-CoV-2, and Their Potential Pathophysiological Significance in COVID-19.International journal of molecular sciences · 2023Review
- Mitochondrial Dysfunction and Apoptosis in Brain Microvascular Endothelial Cells Following Blast Traumatic Brain Injury.Cellular and molecular neurobiology · 2023Article
- Long COVID as a Tauopathy: Of "Brain Fog" and "Fusogen Storms".International journal of molecular sciences · 2023Review
- Statin Use in Relation to COVID-19 and Other Respiratory Infections: Muscle and Other Considerations.Journal of clinical medicine · 2023Review
- Analytical Techniques for Single-Cell Biochemical Assays of Lipids.Annual review of biomedical engineering · 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
- Potential of Nano-Antioxidants and Nanomedicine for Recovery from Neurological Disorders Linked to Long COVID Syndrome.Antioxidants (Basel, Switzerland) · 2023Review
- Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19.International journal of molecular sciences · 2022Review
- Role of SARS-CoV-2 in Modifying Neurodegenerative Processes in Parkinson's Disease: A Narrative Review.Brain sciences · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The SARS-CoV-2 virus is notorious for its neuroinvasive capability, causing multiple neurological conditions. The neuropathology of SARS-CoV-2 is increasingly attributed to mitochondrial dysfunction of brain microglia cells. However, the changes in biochemical content of mitochondria that drive the progression of neuro-COVID remain poorly understood. Here we introduce a Raman microspectrometry approach that enables the molecular profiling of single cellular organelles to characterize the mitochondrial molecular makeup in the infected microglia cells. We found that microglia treated with either spike protein or heat-inactivated SARS-CoV-2 trigger a dramatic reduction in mtDNA content and an increase in phospholipid saturation levels. At the same time, no significant changes were detected in Golgi apparatus and in lipid droplets, the organelles that accommodate biogenesis and storage of lipids. We hypothesize that transformations in mitochondria are caused by increased synthesis of reactive oxygen species in these organelles. Our findings call for the development of mitochondria-targeted therapeutic approaches to limit neuropathology associated with SARS-CoV-2.
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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.