ArticleInternational journal of molecular sciences2021
Inhibition of Lysine 63 Ubiquitination Prevents the Progression of Renal Fibrosis in Diabetic DBA/2J Mice.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Protecting kidney function: from mechanisms to therapeutic targets and traditional Chinese medicine.Renal failure · 2025Review
- Multi-omics integration highlights the role of ubiquitination in endometriosis fibrosis.Journal of translational medicine · 2024Article
- The Role of Non-Coding RNAs in Kidney Diseases.International journal of molecular sciences · 2022Article
- Recent advances in molecular mechanisms of acute kidney injury in patients with diabetes mellitus.Frontiers in endocrinology · 2022Review
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Diabetic nephropathy (DN) is the most frequent cause of end-stage renal disease. Tubulointerstitial accumulation of lysine 63 (K63)-ubiquitinated (Ub) proteins is involved in the progression of DN fibrosis and correlates with urinary miR-27b-3p downregulation. We explored the renoprotective effect of an inhibitor of K63-Ub (NSC697923), alone or in combination with the ACE-inhibitor ramipril, in vitro and in vivo. Proximal tubular epithelial cells and diabetic DBA/2J mice were treated with NSC697923 and/or ramipril. K63-Ub protein accumulation along with α-SMA, collagen I and III, FSP-1, vimentin, p16
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