ArticleInternational urology and nephrology2022
Overexpression of TRIM3 protects against LPS-induced acute kidney injury via repressing IRF3 pathway and NLRP3 inflammasome.
Article in International urology and nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Nephroprotective Effect of L-Carvone on a Mouse Model of LPS-Induced Sepsis-Associated Renal Injury via Regulation of TLR4/NF-κB/AP-1/IRF-3 and Nrf2/iNOS Molecular Signaling Cascades.Journal of Taibah University Medical Sciences · 2026Article
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- The characteristics of extrachromosomal circular DNA in patients with end-stage renal disease.European journal of medical research · 2023Article
- TRIM3 attenuates cytokine storm caused byFrontiers in microbiology · 2023Article
- Article
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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
purposeThe pathological process of sepsis involves multiple system organs, including kidney. Sepsis-induced acute kidney injury (AKI) has high morbidity and high mortality. Overproduced inflammatory factors contribute to the occurrence and evolvement of AKI. Here, the role and underlying mechanism of tripartite motif containing 3 (TRIM3) and in AKI was explored.
methodsLipopolysaccharide (LPS) was used for constructing AKI model both in vitro and in vivo. RT-PCR and western blot were performed to detect TRIM3, Interferon regulatory factor 3 (IRF3) and NLRP3-ASC-Caspase1 inflammasome. Upon selectively regulating the TRIM3 or IRF3 expression, the proliferation, apoptosis and inflammatory response were detected. The interaction between TRIM3 and IRF3 was verified by Immunoprecipitation (IP).
resultsTRIM3 was down-regulated in mediated injury renal tubular epithelial cell line HK-2 treated with LPS. Overexpression of TRIM3 promoted cell viability and reduced apoptosis. In addition, overexpression of TRIM3 inhibited the expression of inflammatory factors (IL-1β, IL-6, TNF-α and IL-18), dampened the phosphorylation of IRF3 and repressed NLRP3 inflammasome activation. Furthermore, TRIM3 overexpression significantly eased the LPS-induced damage on AKI rat model and decreased the serum creatinine and urea nitrogen levels in rat kidney tissues. The results of immunohistochemistry (IHC) and Western blot manifested that TRIM3 was increased dramatically after TRIM3 was overexpressed in the rat kidney tissues, while IRF3 and NLRP3-ASC-Caspase1 inflammasome were significantly repressed following TRIM3 upregulation in the kidney tissues. Mechanistically, TRIM3 interacted with IRF3 and inhibited its phosphorylation.
conclusionOverexpression of TRIM3 protected against LPS-induced AKI by inhibiting the IRF3 pathway and NLRP3 inflammasome activation.
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