ArticleLaboratory investigation; a journal of technical methods and pathology2021
TRIM27 contributes to glomerular endothelial cell injury in lupus nephritis by mediating the FoxO1 signaling pathway.
Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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15 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Article
- TRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease.Cell death discovery · 2026Article
- Genome-Wide Association Studies of Diabetic Kidney Disease in East Asians With Type 2 Diabetes: Achievements and Future Perspectives.Current medicinal chemistry · 2026Review
- The Endothelial Glycocalyx: The First Line of Defense in the Prevention and Treatment of Kidney Diseases.Kidney medicine · 2025Review
- Tri-domain proteins 27 alleviates ischemia-reperfusion injury-induced acute kidney injury by promoting Gli-like transcription factor 1 expression via the inhibition of polycomb repressive complex 2 activity.Journal of cell communication and signaling · 2025Article
- Combined Network Pharmacology, Transcriptomics and Metabolomics Strategies Reveal the Mechanism of Action of Lang Chuang Wan to Ameliorate Lupus Nephritis in MRL/lpr Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Exploring the mechanism by which UCHL3 alleviates diabetic foot ulcers: FOXM1/NLRP3 inflammasome-mediated angiogenesis and endothelial cell pyroptosis.Journal of orthopaedic surgery and research · 2025Article
- Integrated multiomic analyses: An approach to improve understanding of diabetic kidney disease.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- The Mechanism of Hyperglycemia-Induced Renal Cell Injury in Diabetic Nephropathy Disease: An Update.Life (Basel, Switzerland) · 2023Review
- Identification of genetic variants associated with diabetic kidney disease in multiple Korean cohorts via a genome-wide association study mega-analysis.BMC medicine · 2023Article
- Knockdown of TRIM27 alleviated sepsis-induced inflammation, apoptosis, and oxidative stress via suppressing ubiquitination of PPARγ and reducing NOX4 expression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Novel insight into the aetiology of rheumatoid arthritis gained by a cross-tissue transcriptome-wide association study.RMD open · 2022Article
- Endothelial cells: potential novel regulators of renal inflammation.American journal of physiology. Renal physiology · 2022Review
- Emerging roles of TRIM27 in cancer and other human diseases.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif-containing 27 (TRIM27) belongs to the triple motif (TRIM) protein family, which plays a role in a variety of biological activities. Our previous study showed that the TRIM27 protein was highly expressed in the glomerular endothelial cells of patients suffering from lupus nephritis (LN). However, whether TRIM27 is involved in the injury of glomerular endothelial cells in lupus nephritis remains to be clarified. Here, we detected the expression of the TRIM27 protein in glomerular endothelial cells in vivo and in vitro. In addition, the influence of TRIM27 knockdown on endothelial cell damage in MRL/lpr mice and cultured human renal glomerular endothelial cells (HRGECs) was explored. The results revealed that the expression of TRIM27 in endothelial cells was significantly enhanced in vivo and in vitro. Downregulating the expression of TRIM27 inhibited the breakdown of the glycocalyx and the injury of endothelial cells via the FoxO1 pathway. Moreover, HRGECs transfected with the WT-FoxO1 plasmid showed a reduction in impairment caused by LN plasma. Furthermore, suppression of the protein kinase B (Akt) pathway could attenuate damage by mediating the expression of TRIM27. Thus, the present study showed that TRIM27 participated in the injury of glomerular endothelial cells and served as a potential therapeutic target for the treatment of lupus nephritis.
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