ArticleMolecular and cellular biochemistry2023
CircEXOC5 facilitates cell pyroptosis via epigenetic suppression of Nrf2 in septic acute lung injury.
Article in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Bibliometric analysis of pyroptosis in pathogenesis and treatment of acute lung injury.Frontiers in medicine · 2024Pooled it
- Review
- Epigenetics-mediated pathological alterations and their diagnostic and therapeutic potential in sepsis-associated acute kidney injury.Clinical epigenetics · 2026Review
- Circular RNA circVAPA modulates macrophage pyroptosis in sepsis-induced acute lung injury through targeting miR-212-3p/Sirt1/Nrf2/NLRP3 axis.International journal of experimental pathology · 2024Article
- Long Noncoding RNA SOX2OT Ameliorates Sepsis-Induced Myocardial Injury by Inhibiting Cellular Pyroptosis Through Mediating the EZH2/Nrf-2/NLRP3 Signaling Pathway.Journal of inflammation research · 2024Article
- Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury.Frontiers in pharmacology · 2024Review
- lncRNA NEAT1 mediates LPS-induced pyroptosis of BEAS-2B cells via targeting miR-26a-5p/ROCK1 axis.The Kaohsiung journal of medical sciences · 2023Article
- circEXOC5 promotes acute lung injury through the PTBP1/Skp2/Runx2 axis to activate autophagy.Life science alliance · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) caused by sepsis is characterized by a destructive high inflammatory response in lungs, which is the ultimate cause of high mortality to patients diagnosed with sepsis. The objective of the present study is to explore the effect and related mechanisms of circEXOC5 on pyroptosis in septic ALI. Sepsis ALI mouse model was induced and established by CLP induction and sepsis MPVEC cell model by LPS. HE staining was used to detect lung tissue pathological changes. ELISA, flow cytometry, and Western blot were utilized to evaluate the release of inflammatory cytokines and cell pyroptosis, and RIP was applied to verify the binding relationship between EZH2 and circEXOC5 or Nrf2. Finally, the interaction between CircEXOC5 and EZH2, H3k27me3, and Nrf2 promoter regions was clarified using ChIP. CircEXOC5 levels were notably ascended in the lung tissues of septic ALI mice. And silencing circEXOC5 inhibited cell pyroptosis and the release of inflammatory cytokines in MPVEC stimulated by LPS. In addition, RIP and ChIP indicated that Nrf2 expression in MPVECs cells could be inhibited by circEXOC5 via recruiting EZH2. In addition, ML385 (a specific inhibitor of Nrf2) reversed the efficacy of Knockdown of circEXOC5 on the Inhibition of pyroptosis and inflammation of MPVEC cells stimulated by LPS. These results indicated that CircEXOC5 could promote cell pyroptosis through epigenetic inhibition of Nrf2 in septic ALI.
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