ArticleAging2023
Emodin attenuates diabetic kidney disease by inhibiting ferroptosis via upregulating Nrf2 expression.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 24 citations in OpenAlex.
- Ferroptosis inhibition and mitochondrial rescue: a novel mechanism of emodin in rheumatoid arthritis.Redox report : communications in free radical research · 2026Article
- Qigui didang decoction alleviates renal injury in a diabetic kidney disease model with metabolic memory features: association with ferroptosis and the SIRT1/Nrf2 pathway.Pharmaceutical biology · 2026Article
- Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease.World journal of diabetes · 2026Article
- Iron-Driven Ferroptosis in Diabetic Kidney Disease: From Molecular Mechanisms to Targeted Therapeutic Translation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Neutrophil extracellular traps drive osteoporosis via NCF2-dependent signaling: integrated transcriptomics with mechanistic validation.Redox report : communications in free radical research · 2025Article
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Inhibition of SLC3A2 Deletion-Mediated Ferroptosis by Bone Marrow Stromal Cells to Alleviate Inflammation and Fibrosis in Diabetic Kidney Disease.Inflammation · 2025Article
- NRF2 Dysregulation and Therapeutic Insights Across Chronic Kidney Diseases.International journal of molecular sciences · 2025Review
- Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway.Journal of diabetes investigation · 2025Article
- Emodin alleviates the damage to lens epithelial cells in diabetic cataract by repressing the p53-mediated ferroptosis pathway.International ophthalmology · 2025Article
- The gut-kidney axis is regulated by astragaloside IV to inhibit cyclosporine A-induced nephrotoxicity.Frontiers in pharmacology · 2025Article
- Mapping the future: bibliometric insights into ferroptosis and diabetic nephropathy.Frontiers in physiology · 2025Review
- Anthraquinones fromDrug design, development and therapy · 2025Review
- Ferroptosis as a potential therapeutic target for obesity-related metabolic diseases.Frontiers in pharmacology · 2025Review
- Targeting ferroptosis: novel therapeutic approaches and intervention strategies for kidney diseases.Frontiers in immunology · 2025Review
- Elucidating the Mechanism of Jisheng Shenqi Pills in the Treatment of Diabetic Kidney Disease: Network Pharmacology Combined with Experimental Verification.Endocrine, metabolic & immune disorders drug targets · 2025Article
- Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy.Molecular medicine (Cambridge, Mass.) · 2024Review
- Targeting ferroptosis as a prospective therapeutic approach for diabetic nephropathy.Annals of medicine · 2024Review
- Suppression of ferroptosis through the SLC7A11/glutathione/glutathione peroxidase 4 axis contributes to the therapeutic action of the Tangshenning formula on diabetic renal tubular injury.Chinese medicine · 2024Article
- Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis-A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic kidney disease (DKD) poses a threat to people's health. The current treatments only provide partial relief of symptoms. Therefore, seeking a promising therapeutic medication for the prevention and control on DKD will benefit patients. Recently, a novel iron-dependent and non-apoptotic regulated mode of cell death, termed as ferroptosis, is expected to offer us a novel insight into the mechanism of DKD. We conducted experiments to investigate the role of ferroptosis in the development of DKD. Iron accumulation, weakened antioxidant capacity and ROS overproduction were observed in the renal tissues of STZ-induced diabetic rats. A persistent high glucose condition contributed to down regulated levels of Glutathione Peroxidase 4 (GPX4) and Solute Carrier Family 7 Member 11 (SLC7A11) which marked the occurrence of ferroptosis. Treatment of Emodin in DKD models could significantly attenuated these changes and reduced renal injury. Besides, NFE2-related factor 2 (Nrf2), an important antioxidant regulator, was inhibited in both
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