AI Article Synopsis
- Tubulointerstitial fibrosis (TIF) is a key change in diabetic kidney disease, linked to the epithelial‑mesenchymal transition (EMT) of renal tubular cells.
- The study explored how SUMOylation (a type of modification) affects the activity of STAT1, a transcription factor, in the context of high glucose levels leading to EMT.
- Findings revealed that while STAT1 activation offers protection against EMT, increased SUMOylation in high glucose conditions hampers STAT1’s protective role by inhibiting its activity.
Article Abstract
Tubulointerstitial fibrosis (TIF) is an important pathological change that occurs during the development of diabetic kidney disease. The epithelial‑mesenchymal transition (EMT) of renal tubular epithelial cells is a manifestation of TIF. STAT1, a member of the STAT family of transcription factors, can be modified by the small ubiquitin‑related modifier (SUMO), thus affecting the activity of STAT1. The present study investigated the role of STAT1 SUMOylation in high glucose‑induced tubular EMT by western blotting, immunocytochemistry, immunofluorescence, co‑immunoprecipitation and dual luciferase reporter analysis. The results indicated that in the process of high glucose‑induced EMT, STAT1 activation protected the cells from EMT. However, high glucose also increased the SUMOylation of STAT1, which prevented STAT1 from exerting an effective protective role by inhibiting its activity.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9835054 | PMC |
| http://dx.doi.org/10.3892/mmr.2023.12929 | DOI Listing |
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