ArticleJournal of diabetes investigation2024
Tanshinone IIA suppresses ferroptosis to attenuate renal podocyte injury in diabetic nephropathy through the embryonic lethal abnormal visual-like protein 1 and acyl-coenzyme A synthetase long-chain family member 4 signaling pathway.
Article in Journal of diabetes investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.
- Efficacy and safety of Jinlida granules as an adjuvant treatment for diabetic nephropathy: a systematic review and meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Lipid Peroxidation in Diabetic Kidney Disease: Mechanism and Natural Solution.International journal of molecular sciences · 2025Pooled it
- The ELAVL1-PLAUR-suPAR Axis Exacerbates Diabetic Nephropathy by Promoting Podocyte Injury and Inflammation.Journal of diabetes · 2026Article
- Review
- The "habitat-phytochemistry-pharmacological effect" nexus: a multidimensional review of ethnomedicinalFrontiers in pharmacology · 2026Review
- Iron-Driven Ferroptosis in Diabetic Kidney Disease: From Molecular Mechanisms to Targeted Therapeutic Translation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Natural Products as Potential Therapeutic Candidates for Diabetic Kidney Disease: Molecular Mechanisms, Translational Challenges, and Future Prospects.International journal of molecular sciences · 2025Review
- Review
- The Inflammatory Cell Death in Diabetic Kidney Disease: Integrating Multifactorial Mechanisms into Novel Therapeutics.International journal of molecular sciences · 2025Review
- Natural Products as Modulators of Iron Metabolism and Ferroptosis in Diabetes and Its Complications.Nutrients · 2025Review
- ELAVL1 promotes ferroptosis via the TRIM21/HOXD8 axis to inhibit osteogenic differentiation in congenital pseudoarticular tibia-derived mesenchymal stem cells.Journal of cell communication and signaling · 2025Article
- Article
- Calcium/Calmodulin-Dependent Protein Kinase II β Regulates Autophagy Dependent Ferroptosis of Neurons after Cerebral Ischemic Injury by Activating the AREG/JUN/ELAVL1 Pathway.Neurochemical research · 2025Article
- Upregulation of SQSTM1 Regulates Ferroptosis and Oxidative Stress in Müller Cells of the Diabetic Neural Retina by Modulating ACSL4.Journal of diabetes research · 2025Article
- Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy.Molecular medicine (Cambridge, Mass.) · 2024Review
- Podocyte Death in Diabetic Kidney Disease: Potential Molecular Mechanisms and Therapeutic Targets.International journal of molecular sciences · 2024Review
- Therapeutic effects of natural compounds against diabetic complications via targeted modulation of ferroptosis.Frontiers in pharmacology · 2024Review
- Autophagy Regulates Ferroptosis-Mediated Diabetic Liver Injury by Modulating the Degradation of ACSL4.Journal of diabetes research · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
AIMS/
introductionTanshinone IIA (TIIA) is one of the main components of the root of the red-rooted Salvia miltiorrhiza Bunge. However, the molecular mechanisms underlying TIIA-mediated protective effects in diabetic nephropathy (DN) are still unclear. MATERIALS AND
methodsHigh glucose (HG)-induced mouse podocyte cell line (MPC5) cells were used as the in vitro model of DN and treated with TIIA. Cell viability, proliferation and apoptosis were detected using 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide, 5-ethynyl-2'-deoxyuridine and flow cytometry assays. The protein levels were assessed using western blot assay. The levels of inflammatory factors were deleted by enzyme-linked immunoassay. Fe
resultsTIIA repressed HG-induced MPC5 cell apoptosis, inflammatory response and ferroptosis. ACSL4 upregulation relieved the repression of TIIA on HG-mediated MPC5 cell injury and ferroptosis. ELAVL1 is bound with ACSL4 to positively regulate the stability of ACSL4 messenger ribonucleic acid. TIIA hindered HG-triggered MPC5 cell injury and ferroptosis by regulating the ELAVL1-ACSL4 pathway. TIIA blocked DN progression in in vivo research.
conclusionTIIA treatment restrained HG-caused MPC5 cell injury and ferroptosis partly through targeting the ELAVL1-ACSL4 axis, providing a promising therapeutic target for DN treatment.
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