ArticleLife science alliance2023
Inhibition of the SREBP pathway prevents SARS-CoV-2 replication and inflammasome activation.
Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Neutrophil extracellular traps promote macrophage activation through Toll-like receptor engagement and PKA and NF-kB signaling pathways.Cell communication and signaling : CCS · 2026Article
- Behind the membranous curtain-lipid dynamics and functions in coronaviral replication.Journal of virology · 2026Review
- Spatial transcriptomics and single-nucleus RNA sequencing reveal rAAV2- and rAAV9-specific transduction signatures in the mouse liver.Gene therapy · 2026Article
- Multiorgan Molecular Landscape of Severe COVID-19 Revealed by Consensus Gene Signatures and RAB8B Targeting.Journal of medical virology · 2026Article
- Article
- Serum lipidome remodeling in viral pneumonia: from pathophysiology to therapeutics.Frontiers in immunology · 2026Review
- Airway immunometabolic responses during pulmonary bacterial and viral infections.Cell reports · 2025Review
- Interplay Between NLRP3 Activation by DENV-2 and Autophagy and Its Impact on Lipid Metabolism in HMEC-1 Cells.Pathogens (Basel, Switzerland) · 2025Article
- SREBP2-dependent lipid droplet formation enhances viral replication and deteriorates lung injury in mice following IAV infection.Emerging microbes & infections · 2025Article
- Profiles of PCSK9, SREBP-2, and histopathology in COVID-19 and non-COVID-19 critical illness.BMC infectious diseases · 2025Article
- Influenza virus infection reprograms cholesterol biosynthesis to facilitate virus replication by the TAK1-RORγ axis.PLoS pathogens · 2025Article
- From fat to fire: The lipid-inflammasome connection.Immunological reviews · 2025Review
- SARS-CoV-2 exploits steroidogenic machinery, triggers lipid metabolism for viral replication and induces immune response in Leydig cells of K18-hACE2 mice.Frontiers in cellular and infection microbiology · 2025Article
- Review
- Lipid Droplets: Formation, Degradation, and Their Role in Cellular Responses to Flavivirus Infections.Microorganisms · 2024Review
- Consequences of COVID-19 on Adipose Tissue Signatures.International journal of molecular sciences · 2024Article
- Lipid Metabolism Modulation during SARS-CoV-2 Infection: A Spotlight on Extracellular Vesicles and Therapeutic Prospects.International journal of molecular sciences · 2024Review
- The effects of iron deficient and high iron diets on SARS-CoV-2 lung infection and disease.Frontiers in microbiology · 2024Article
- Advances in research on the impact and mechanisms of pathogenic microorganism infections on pyroptosis.Frontiers in microbiology · 2024Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 induces major cellular lipid rearrangements, exploiting the host's metabolic pathways to replicate. Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that control lipid metabolism. SREBP1 is associated with the regulation of fatty acids, whereas SREBP2 controls cholesterol metabolism, and both isoforms are associated with lipid droplet (LD) biogenesis. Here, we evaluated the effect of SREBP in a SARS-CoV-2-infected lung epithelial cell line (Calu-3). We showed that SARS-CoV-2 infection induced the activation of SREBP1 and SREBP2 and LD accumulation. Genetic knockdown of both SREBPs and pharmacological inhibition with the dual SREBP activation inhibitor fatostatin promote the inhibition of SARS-CoV-2 replication, cell death, and LD formation in Calu-3 cells. In addition, we demonstrated that SARS-CoV-2 induced inflammasome-dependent cell death by pyroptosis and release of IL-1β and IL-18, with activation of caspase-1, cleavage of gasdermin D1, was also reduced by SREBP inhibition. Collectively, our findings help to elucidate that SREBPs are crucial host factors required for viral replication and pathogenesis. These results indicate that SREBP is a host target for the development of antiviral strategies.
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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.