ArticleCells2022
The Spike Protein of SARS-CoV-2 Impairs Lipid Metabolism and Increases Susceptibility to Lipotoxicity: Implication for a Role of Nrf2.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 27 citations in OpenAlex.
- SARS-CoV-2 Spike Protein Induces Time-Dependent and Brain-Region-Specific Alterations in Ferroptosis Markers: A Preliminary Study in K18-hACE2 Mice.International journal of molecular sciences · 2026Article
- Recent progress in understanding ferroptosis mechanisms in infectious diseases.Frontiers in cellular and infection microbiology · 2026Review
- Review
- Hepatic Metabolic Dysregulation as a Potential Amplifier of Leukemogenesis Following mRNA Vaccination: A Novel Mechanistic Hypothesis.Medicina (Kaunas, Lithuania) · 2025Article
- Nuclear Factor Erythroid 2-Related Factor 2 and SARS-CoV-2 Infection Risk in COVID-19-Vaccinated Hospital Nurses.Vaccines · 2025Article
- Plasma miR-1-3p levels predict severity in hospitalized COVID-19 patients.British journal of pharmacology · 2025Article
- The role and therapeutic potential of itaconate in lung disease.Cellular & molecular biology letters · 2024Review
- The Role of the Nrf2 Pathway in Airway Tissue Damage Due to Viral Respiratory Infections.International journal of molecular sciences · 2024Review
- Pharmacological Activities, Therapeutic Effects, and Mechanistic Actions of Trigonelline.International journal of molecular sciences · 2024Review
- Immunogenicity studies of recombinant RBD SARS-CoV-2 as a COVID-19 vaccine candidate produced inVaccine: X · 2024Article
- Human PBMCs Form Lipid Droplets in Response to Spike Proteins.Microorganisms · 2023Article
- SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway.Cell stress & chaperones · 2023Review
- The SARS-CoV-2 Spike protein induces long-term transcriptional perturbations of mitochondrial metabolic genes, causes cardiac fibrosis, and reduces myocardial contractile in obese mice.bioRxiv : the preprint server for biology · 2023Article
- Uptake of severe acute respiratory syndrome coronavirus 2 spike protein mediated by angiotensin converting enzyme 2 and ganglioside in human cerebrovascular cells.Frontiers in neuroscience · 2023Article
- Lipid Nanoparticles and Liposomes for Bone Diseases Treatment.Biomedicines · 2022Review
- Autophagy Dysregulation in Metabolic Associated Fatty Liver Disease: A New Therapeutic Target.International journal of molecular sciences · 2022Review
- Untargeted plasma metabolomic fingerprinting highlights several biomarkers for the diagnosis and prognosis of coronavirus disease 19.Frontiers in medicine · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Coronavirus disease 2019 (COVID-19) patients show lipid metabolic alterations, but the mechanism remains unknown. In this study, we aimed to investigate whether the Spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) impairs lipid metabolism in host cells. We generated a Spike cell line in HEK293 using the pcDNA vector carrying the Spike gene expression cassette. A control cell line was generated using the empty pcDNA vector. Gene expression profiles related to lipid metabolic, autophagic, and ferroptotic pathways were investigated. Palmitic acid (PA)-overload was used to assess lipotoxicity-induced necrosis. As compared with controls, the Spike cells showed a significant increase in lipid depositions in cell membranes as well as dysregulation of expression of a panel of molecules involving lipid metabolism, autophagy, and ferroptosis. The Spike cells showed an upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2), a multifunctional transcriptional factor, in response to PA. Furthermore, the Spike cells exhibited increased necrosis in response to PA-induced lipotoxicity compared to control cells in a time- and dose-dependent manner via ferroptosis, which could be attenuated by the Nrf2 inhibitor trigonelline. We conclude that the Spike protein impairs lipid metabolic and autophagic pathways in host cells, leading to increased susceptibility to lipotoxicity via ferroptosis which can be suppressed by a Nrf2 inhibitor. This data also suggests a central role of Nrf2 in Spike-induced lipid metabolic impairments.
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Registered trials
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