ArticleInternational journal of biological sciences2024
Ursolic Acid Alleviates Mitotic Catastrophe in Podocyte by Inhibiting Autophagic P62 Accumulation in Diabetic Nephropathy.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed.
- Tubular PFKFB3 drives diabetic kidney fibrosis via lactate‑dependent H4K12 lactylation and HIPK2 transactivation.International journal of molecular medicine · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease.World journal of diabetes · 2026Article
- Review
- Delactylase effects of SIRT3 on a positive feedback loop involving the RUNX1-glycolysis-histone lactylation in diabetic kidney disease.International journal of biological sciences · 2026Article
- Association between the serum uric acid-to-high-density lipoprotein cholesterol ratio and microalbuminuria in individuals with type 2 diabetes mellitus.European journal of medical research · 2025Article
- Podocytes in health and disease: from development to regeneration.Human cell · 2025Review
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Diagnostic value of the correlation between urinary MDM2 and podocyte mitotic catastrophe in diabetic kidney disease.Diabetology & metabolic syndrome · 2025Article
- Network Pharmacology, Molecular Dynamics Simulation, and Biological Validation Insights into the Potential of Ligustri Lucidi Fructus for Diabetic Nephropathy.International journal of molecular sciences · 2025Article
- The Impact of METTL3 on MDM2 Promotes Podocytes Injury During Diabetic Kidney Disease.Journal of cellular and molecular medicine · 2025Article
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Research on podocyte injury mechanisms in diabetic nephropathy: a bibliometric and knowledge-map analysis from 2000 to 2024.Frontiers in endocrinology · 2025Article
- Rhubarb: Traditional Uses, Phytochemistry, Multiomics-Based Novel Pharmacological and Toxicological Mechanisms.Drug design, development and therapy · 2025Review
- [Inhibition of miR-30d-5p promotes mitochondrial autophagy and alleviates high glucose-induced injury in podocytes].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Article
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7 authors.
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Abstract
The glomerular podocyte, a terminally differentiated cell, is crucial for the integrity of the glomerular filtration barrier. The re-entry of podocytes into the mitotic phase results in injuries or death, known as mitotic catastrophe (MC), which significantly contributes to the progression of diabetic nephropathy (DN). Furthermore, P62-mediated autophagic flux has been shown to regulate DN-induced podocyte injury. Although previous studies, including ours, have demonstrated that ursolic acid (UA) mitigates podocyte injury by enhancing autophagy under high glucose conditions, the protective functions and potential regulatory mechanisms of UA against DN have not been fully elucidated. For aiming to investigate the regulatory mechanism of podocyte injuries in DN progression, and the protective function of UA treatment against DN progression, we utilized db/db mice and high glucose (HG)-induced podocyte models in vivo and in vitro, with or without UA administration. Our findings indicate that UA treatment reduced DN progression by improving biochemical indices. P62 accumulation led to Murine Double Minute gene 2 (MDM2)-regulated MC in podocytes during DN, which was ameliorated by UA through enhanced P62-mediated autophagy. Additionally, the overexpression of NF-κB p65 or TNF-α abolished the protective effects of UA both
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