ArticleFrontiers in cell and developmental biology2020
Icariin Prevents Extracellular Matrix Accumulation and Ameliorates Experimental Diabetic Kidney Disease by Inhibiting Oxidative Stress via GPER Mediated p62-Dependent Keap1 Degradation and Nrf2 Activation.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 63 citations in OpenAlex.
- Randomized controlled clinical trial of Shenzhuo Formula in the treatment of macroalbuminuria in diabetic kidney disease and its inflammation-modulating mechanisms.Precision clinical medicine · 2025Trial
- Natural product therapy in diabetic kidney disease: emerging multiomics-mediated signalling pathway and molecular target.Chinese medicine · 2026Review
- Icariin Attenuates Renal Injury in Streptozotocin-Induced Diabetic Rats with and Without Adenine-Induced Chronic Kidney Disease.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Polyphenol-Mediated Modulation of Oxidative Stress Pathways in Type 1 Diabetes: A Systematic Review.Antioxidants (Basel, Switzerland) · 2026Review
- Icariin protects against cisplatin-induced renal injury and ferroptosis via JNK pathway in mice.BMC nephrology · 2026Article
- Inflammation, Apoptosis, and Fibrosis in Diabetic Nephropathy: Molecular Crosstalk in Proximal Tubular Epithelial Cells and Therapeutic Implications.Current issues in molecular biology · 2025Review
- GPER in metabolic homeostasis and disease: molecular mechanisms, nutritional regulation, and therapeutic potential.Journal of translational medicine · 2025Review
- NRF2 Dysregulation and Therapeutic Insights Across Chronic Kidney Diseases.International journal of molecular sciences · 2025Review
- Expression and Regulatory Roles of SKAP2 and Cortactin in Mouse Ovarian Tissue and Oocyte Maturation.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Preclinical evidence of the effect of icariin on diabetic nephropathy: a systematic review and meta-analysis.Diabetology & metabolic syndrome · 2025Review
- Oxidative Stress Induced by Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) Dysfunction Aggravates Chronic Inflammation Through the NADAntioxidants (Basel, Switzerland) · 2025Review
- Therapeutic Effects and Mechanisms of Icaritin in Parkinson's Disease.Current pharmaceutical design · 2025Review
- Pharmacological potential of Chinese botanical drugs in managing chronic kidney disease by targeting mitochondrial quality control.Frontiers in pharmacology · 2025Review
- Natural small molecules regulating the mitophagy pathway counteract the pathogenesis of diabetes and chronic complications.Frontiers in pharmacology · 2025Review
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
- Icariin alleviates cisplatin-induced premature ovarian failure by inhibiting ferroptosis through activation of the Nrf2/ARE pathway.Scientific reports · 2024Article
- The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Mechanisms and efficacy of traditional Chinese herb monomers in diabetic kidney disease.International urology and nephrology · 2024Review
- Global research hotspots and trends in oxidative stress-related diabetic nephropathy: a bibliometric study.Frontiers in endocrinology · 2024Article
- Advances in oxidative stress in pathogenesis of diabetic kidney disease and efficacy of TCM intervention.Renal failure · 2023Review
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7 authors at 1 institution in 1 country.
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Abstract
The present study aimed to determine whether icariin could attenuate type 1 diabetic nephropathy (T1DN) induced by streptozotocin (STZ) after 4 weeks or not. Therefore, its therapeutic effect on diabetic kidney disease was investigated in view of reactive oxygen (ROS) and extracellular matrix (ECM) generation in human glomerular mesangial cells under high glucose. To establish the participation and the key role of GPER and Nrf2 in ECM deposition, a combination of G15 (antagonist of GPER) or siGPER and siNrf2 were performed, respectively. The results showed that T1DN can be significantly inhibited by oral icariin, evidenced by improvement of 24 h urinary volume, 24 h proteinuria, microalbuminuria, and histopathological changes of kidney. Icariin decreased the levels of intracellular superoxide anion, impeded the generation of fibronectin and increased the expression and activity of antioxidant enzymes in the human glomerular mesangial cells treated with high glucose. It acted as a GPER activator, increased dissociation of Nrf2/Keap1 complexes, combination of Keap1/p62 complexes, Nrf2 translocation to nuclear, Nrf2/ARE DNA binding activity, and ARE luciferase reporter gene activity in glomerular mesangial cells. The Nrf2 inhibitor ML385 or siNrf2 obviously abolished extracellular matrix (ECM) generation inhibited by icariin. Furthermore, icariin-induced Nrf2 activation was mainly dependent on p62-mediated Keap1 degradation, which functions as an adaptor protein during autophagy. The GPER antagonist G15 and siGPER obviously abolished the above effects by icariin. Taken together, the present study demonstrated that the therapeutic effects of icariin on type 1 diabetic nephropathy in rats via GPER mediated p62-dependent Keap1 degradation and Nrf2 activation.
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