ArticleCell death and differentiation2022
SARS-CoV-2 membrane protein causes the mitochondrial apoptosis and pulmonary edema via targeting BOK.
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 89 citations in OpenAlex.
- SIRT1/AMPK/PGC1α pathway in ischemic stroke: Elucidating neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Disruption of ER-mitochondria contact sites by coronavirus replication organelles sustains viral replication via NSP3 stabilization.The EMBO journal · 2026Article
- Exploring Key Regulators of Mitochondrial Dynamics and Immune Response in SARS-CoV-2 Infection.Viruses · 2026Article
- Potential causal role of mitochondrial biological effects in COVID-19: Evidence from Mendelian randomization study.Medicine · 2026Article
- Comparative progress on the mechanisms of airway mucosal injury induced by different pathogens: SARS-CoV-2, influenza A virus, and Mycoplasma pneumoniae.Frontiers in cellular and infection microbiology · 2026Review
- Gastrodin alleviates high fructose-induced podocyte mitochondria-mediated apoptosis by inhibiting NLRP6 to facilitate TRIM7-triggeredInternational journal of biological sciences · 2026Article
- The structure and function of membrane protein in coronavirus infection and its applications in the development of vaccines and therapeutic drugs.Frontiers in microbiology · 2026Review
- SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteins.Emerging microbes & infections · 2025Article
- The NSP5, ORF6 and NSP13 of SARS-CoV-2 Cooperate to Modulate Inflammatory Cell Death Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Different Susceptibility of Mammalian Cell Lines to Severe Fever with Thrombocytopenia Syndrome Virus Infection.Viruses · 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
- Mitochondrial Reactive Oxygen Species: A Unifying Mechanism in Long COVID and Spike Protein-Associated Injury: A Narrative Review.Biomolecules · 2025Review
- Sivelestat sodium: a novel therapeutic agent in a mouse model of acute exacerbation pulmonary fibrosis through multiple mechanisms.Journal of thoracic disease · 2025Article
- Production of SARS-CoV-2 virus-like particles as a vaccine candidate in stable cell lines through inducible E and M protein expression.BMC biotechnology · 2025Article
- Low BOK Expression Promotes Epithelial-Mesenchymal Transition and Migration via the Wnt Signaling Pathway in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
- Mitochondrial haplogroup A2 is associated with increased COVID-19 mortality in an admixed Brazilian population.Scientific reports · 2025Article
- The role of programmed cell death in organ dysfunction induced by opportunistic pathogens.Critical care (London, England) · 2025Review
- Role of mitochondria-associated membranes (MAMs) in inflammatory signaling: implications for acute lung injury pathogenesis.Frontiers in cell and developmental biology · 2025Review
- Quantitative IgG response to SARS-CoV-2 membrane protein in infected individuals strongly correlates with lung injury.Scientific reports · 2024Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deaths caused by coronavirus disease 2019 (COVID-19) are largely due to the lungs edema resulting from the disruption of the lung alveolo-capillary barrier, induced by SARS-CoV-2-triggered pulmonary cell apoptosis. However, the molecular mechanism underlying the proapoptotic role of SARS-CoV-2 is still unclear. Here, we revealed that SARS-CoV-2 membrane (M) protein could induce lung epithelial cells mitochondrial apoptosis. Notably, M protein stabilized B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) via inhibiting its ubiquitination and promoted BOK mitochondria translocation. The endodomain of M protein was required for its interaction with BOK. Knockout of BOK by CRISPR/Cas9 increased cellular resistance to M protein-induced apoptosis. BOK was rescued in the BOK-knockout cells, which led to apoptosis induced by M protein. M protein induced BOK to trigger apoptosis in the absence of BAX and BAK. Furthermore, the BH2 domain of BOK was required for interaction with M protein and proapoptosis. In vivo M protein recombinant lentivirus infection induced caspase-associated apoptosis and increased alveolar-capillary permeability in the mouse lungs. BOK knockdown improved the lung edema due to lentivirus-M protein infection. Overall, M protein activated the BOK-dependent apoptotic pathway and thus exacerbated SARS-CoV-2 associated lung injury in vivo. These findings proposed a proapoptotic role for M protein in SARS-CoV-2 pathogenesis, which may provide potential targets for COVID-19 treatments.
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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.