ArticleBioMed research international2014
High glucose induces sumoylation of Smad4 via SUMO2/3 in mesangial cells.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- SUMO2-mediated SP1 SUMOylation promotes M2 macrophage polarization to facilitate diabetic foot ulcer healing.Molecular and cellular biochemistry · 2026Article
- Targeting posttranslational modifications of oxidative stress pathways for the treatment of diabetic nephropathy.Journal of pharmaceutical analysis · 2026Review
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Ginkgolic acid attenuates echinococcus granulosus infection-induced hepatic fibrosis by inhibiting Smad4 SUMOylation.PLoS neglected tropical diseases · 2026Article
- Enzymatic post-translational modifications of proteins in chronic kidney disease: mechanisms, regulation, and clinical significance.Frontiers in pharmacology · 2025Review
- TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review).Molecular medicine reports · 2024Review
- Exploring potential targets for natural product therapy of DN: the role of SUMOylation.Frontiers in pharmacology · 2024Review
- ATBF1 is a potential diagnostic marker of histological grade and functions via WNT5A in breast cancer.BMC cancer · 2022Article
- Exploration of autoantibody responses in canine diabetes using protein arrays.Scientific reports · 2022Article
- Micro ribonucleic acid-363 regulates the phosphatidylinositol 3-kinase/threonine protein kinase axis by targeting NOTCH1 and forkhead box C2, leading to hepatic glucose and lipids metabolism disorder in type 2 diabetes mellitus.Journal of diabetes investigation · 2022Article
- Natural Products Against Renal FibrosisFrontiers in pharmacology · 2022Review
- Ginkgolic acid improves bleomycin-induced pulmonary fibrosis by inhibiting SMAD4 SUMOylation.Oxidative medicine and cellular longevity · 2022Article
- Regulation of SUMOylation Targets Associated With Wnt/β-Catenin Pathway.Frontiers in oncology · 2022Review
- Regulation of transforming growth factor-β signalling by SUMOylation and its role in fibrosis.Open biology · 2021Article
- Progress of small ubiquitin-related modifiers in kidney diseases.Chinese medical journal · 2019Review
- Deciphering the SUMO code in the kidney.Journal of cellular and molecular medicine · 2019Review
- Review
- Protein Modifications as Manifestations of Hyperglycemic Glucotoxicity in Diabetes and Its Complications.Biochemistry insights · 2016Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that sumoylation is a posttranslational modification involved in regulation of the transforming growth factor-β (TGF-β) signaling pathway, which plays a critical role in renal fibrosis in diabetic nephropathy (DN). However, the role of sumoylation in the regulation of TGF-β signaling in DN is still unclear. In the present study, we investigated the expression of SUMO (SUMO1 and SUMO2/3) and Smad4 and the interaction between SUMO and Smad4 in cultured rat mesangial cells induced by high glucose. We found that SUMO1 and SUMO2/3 expression was significantly increased in the high glucose groups compared to the normal group (P < 0.05). Smad4 and fibronectin (FN) levels were also increased in the high glucose groups in a dose-dependent manner. Coimmunoprecipitation and confocal laser scanning revealed that Smad4 interacted and colocalized with SUMO2/3, but not with SUMO1 in mesangial cells. Sumoylation (SUMO2/3) of Smad4 under high glucose condition was strongly enhanced compared to normal control (P < 0.05). These results suggest that high glucose may activate TGF- β/Smad signaling through sumoylation of Samd4 by SUMO2/3 in mesangial cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.