ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022
Knockdown of TRIM27 alleviated sepsis-induced inflammation, apoptosis, and oxidative stress via suppressing ubiquitination of PPARγ and reducing NOX4 expression.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 14 citations in OpenAlex.
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- O‑GlcNAcylation: The crosstalk between infection immunity and autophagy in sepsis (Review).Molecular medicine reports · 2025Review
- Asiaticoside Mitigates Chronic Obstructive Pulmonary Disease by Modulating TRIM27 Stability and Activating PGC-1α/Nrf2 Signaling.Applied biochemistry and biotechnology · 2025Article
- Review
- TRIM11 modulates sepsis progression by promoting HOXB9 ubiquitination and inducing the NF-κB signaling pathway.Molecular biology reports · 2025Article
- Post-translational modifications in sepsis-induced organ dysfunction: mechanisms and implications.Frontiers in immunology · 2024Review
- Therapeutic potential ofFrontiers in pharmacology · 2023Article
- Idebenone reduces sepsis-induced oxidative stress and apoptosis in hepatocytes via RAGE/p38 signaling.Annals of translational medicine · 2022Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundSepsis is a global fatal disease and leads to severe lung injury due to dysfunction of inflammation response. TRIM27 is closely related to the diseased with dysfunction of inflammation response. The aim of this study was to clarify the role and mechanism of TRIM27 in sepsis-induced lung injury.
methodsThe lipopolysaccharide (LPS)-induced septic mouse model was successfully established. The lung injury was evaluated by lung wet/dry (W/D) ratio and hematoxylin-eosin (H&E) staining. The cell apoptosis was evaluated by TUNEL assay. The inflammatory cytokines were measured by quantitative real time-PCR (qRT-PCR) assay and commercial enzyme-linked immunosorbent assay (ELISA). The oxidative stress was assessed by the contents of superoxide dismutase (SOD) and malondialdehyde (MDA), and the expression of dihydroethidium (DHE).
resultsIn this study, we demonstrated that TRIM27 was up-regulated in LPS-induced septic mice. In loss-of-function experiments, knockdown of TRIM27 alleviated sepsis-induced lung injury, inflammation, apoptosis, and oxidative stress. More importantly, knockdown of TRIM27 was observed to reduce p-p65/NOX4 expression via suppressing ubiquitination of PPARγ. In rescue experiments, overexpression of NOX4 abolished the effect of sh-TRIM27 on alleviating sepsis-induced inflammation, apoptosis, and oxidative stress.
conclusionThese findings highlighted that knockdown of TRIM27 alleviated sepsis-induced inflammation, oxidative stress and apoptosis via suppressing ubiquitination of PPARγ and reducing NOX4 expression, which supports the potential utility of TRIM27 as a therapeutic target in septic lung injury.
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