ReviewCureus2022
Mitogen Activated Protein Kinase (MAPK) Activation, p53, and Autophagy Inhibition Characterize the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike Protein Induced Neurotoxicity.
Review in Cureus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- EpCAM deficiency causes the inflammation of lungs due to the reduction of pIgR in airway epithelium.Respiratory research · 2026Article
- Evaluation of artificial intelligence identified ipratropium bromide for the treatment of coronavirus disease 2019.Scientific reports · 2026Article
- Artificial Intelligence Approach in Machine Learning-Based Modeling and Networking of the Coronavirus Pathogenesis Pathway.Current issues in molecular biology · 2025Article
- Identification of gene signatures and potential pharmaceutical candidates linked to COVID-19-related depression based on gene expression profiles.Frontiers in pharmacology · 2025Article
- Accelerated tumor progression after COVID-19 infection in patients with glioblastoma: A retrospective case-control study.Neuro-oncology practice · 2024Article
- Promising Strategies to Reduce the SARS-CoV-2 Amyloid Deposition in the Brain and Prevent COVID-19-Exacerbated Dementia and Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration.Molecular neurodegeneration · 2024Review
- Review
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- The exploration of glucocorticoid pathway based on disease severity in COVID-19 patients.Heliyon · 2024Article
- Clinical rationale for dietary lutein supplementation in long COVID and mRNA vaccine injury syndromes.F1000Research · 2024Review
- 'Spikeopathy': COVID-19 Spike Protein Is Pathogenic, from Both Virus and Vaccine mRNA.Biomedicines · 2023Review
- mRNA: Vaccine or Gene Therapy? The Safety Regulatory Issues.International journal of molecular sciences · 2023Review
- Roles of p53-Mediated Host-Virus Interaction in Coronavirus Infection.International journal of molecular sciences · 2023Review
- A Potential Role of the Spike Protein in Neurodegenerative Diseases: A Narrative Review.Cureus · 2023Review
- SARS-CoV-2 amyloid, is COVID-19-exacerbated dementia an amyloid disorder in the making?Frontiers in dementia · 2023Article
- Self-DNA driven inflammation in COVID-19 and after mRNA-based vaccination: lessons for non-COVID-19 pathologies.Frontiers in immunology · 2023Article
- Identifying the Potential of miRNAs inInternational journal of nanomedicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein and prions use common pathogenic pathways to induce toxicity in neurons. Infectious prions rapidly activate the p38 mitogen activated protein kinase (MAPK) pathway, and SARS-CoV-2 spike proteins rapidly activate both the p38 MAPK and c-Jun NH2-terminal kinase (JNK) pathways through toll-like receptor signaling, indicating the potential for similar neurotoxicity, causing prion and prion-like disease. In this review, we analyze the roles of autophagy inhibition, molecular mimicry, elevated intracellular p53 levels and reduced Wild-type p53-induced phosphatase 1 (Wip1) and dual-specificity phosphatase (DUSP) expression in neurons in the disease process. The pathways induced by the spike protein via toll-like receptor activation induce both the upregulation of PrP
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What OpenQuestion holds
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.