ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021
Emodin Ameliorates Renal Damage and Podocyte Injury in a Rat Model of Diabetic Nephropathy via Regulating AMPK/mTOR-Mediated Autophagy Signaling Pathway.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Pooled it
- [Poricoic acid A alleviates dextran sulfate sodium-induced colitis in mice by regulating AMPK/mTOR-mediated autophagy and inhibiting intestinal epithelial cell apoptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- The Mechanism and Application of Traditional Chinese Medicine Nano-Formulations in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Natural Products as Potential Therapeutic Candidates for Diabetic Kidney Disease: Molecular Mechanisms, Translational Challenges, and Future Prospects.International journal of molecular sciences · 2025Review
- Article
- The Pathogenesis of Chronic Kidney Disease (CKD) and the Preventive and Therapeutic Effects of Natural Products.Current issues in molecular biology · 2025Review
- Protective efficacy of emodin in Swiss Albino mice induced with Dalton Ascitic lymphoma.3 Biotech · 2025Article
- Vincamine induces cytoprotective autophagy via regulation of ampk/mtor signaling pathway in gentamicin-induced hepatotoxicity and nephrotoxicity in rats.Scientific reports · 2025Article
- mTOR pathway: A key player in diabetic nephropathy progression and therapeutic targets.Genes & diseases · 2025Review
- Renal Implications of Dysregulated Protein Homeostasis: Insights into Ubiquitin-Proteasome and Autophagy Systems.Biomolecules · 2025Review
- Network pharmacology-based study on the mechanism of Tangfukang formula against type 2 diabetes mellitus.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Dapagliflozin restores autophagy and attenuates apoptosis via the AMPK/mTOR pathway in diabetic nephropathy rats and high glucose-induced HK-2 cells.International urology and nephrology · 2025Article
- Immunomodulatory roles of quercetin in diabetic nephropathy: targeting inflammation, oxidative stress, and ferroptosis.Frontiers in pharmacology · 2025Review
- Anthraquinones fromDrug design, development and therapy · 2025Review
- Natural products in traditional Chinese medicine for renal fibrosis: a comprehensive review.Frontiers in pharmacology · 2025Review
- mTOR-mediated nutrient sensing and oxidative stress pathways regulate autophagy: a key mechanism for traditional Chinese medicine to improve diabetic kidney disease.Frontiers in pharmacology · 2025Review
- Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy.Molecular medicine (Cambridge, Mass.) · 2024Review
- Poricoic acid a ameliorates high glucose-induced podocyte injury by regulating the AMPKα/FUNDC1 pathway.Molecular biology reports · 2024Article
- Targeting autophagy with natural products as a potential therapeutic approach for diabetic microangiopathy.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe activation of autophagy has potential protective effect on diabetic nephropathy (DN) podocyte injury, and the AMPK/mTOR signaling pathway is an important regulatory pathway of autophagy. Emodin has been reported to effectively delay DN progression; however, the therapeutic mechanisms involved in vivo remain ambiguous. The present study aimed to elucidate the mechanism of emodin in improving renal tissue and podocyte injury in DN by regulating the AMPK/mTOR-autophagy signaling pathway.
methodsAll rats were divided into 4 groups: a Sham group, a Vehicle group, a low-dose emodin (LD-Emo) group (20 mg/kg/day) and a high-dose emodin (HD-Emo) group (40 mg/kg/day). The different doses of Emo and distilled water were daily administrated for 8 weeks after the induction of DN by the unilateral nephrectomy combined with intraperitoneal injections of streptozotocin (STZ). The rats' general status, blood glucose, biochemical parameters, urinary protein excretion, renal histological changes and cell apoptosis in renal tissue, as well as the key protein expressions in the AMPK/mTOR signaling pathway and apoptosis-related proteins were examined, respectively.
resultsEmodin ameliorated the general condition, kidney weight and urinary protein excretion of the rats, but has little influence on serum biochemical parameters and did not lower blood glucose; emodin attenuated renal fibrosis including the cell numbers, extracellular matrix rate and collagen area in glomerulus, simultaneously relieved podocyte foot process fusion, up-regulated the expression of nephrin protein and suppressed glomerular and tubular epithelial cell apoptosis. In addition, emodin can induce and enhance autophagy in podocytes including increased expression of LC3-II/I, Beclin-1, p-AMPK protein and decreased expression of p62, p-mTOR protein, as well as increased autophagosomes in podocytes.
conclusionWe have demonstrated that emodin, as a natural regulator in vivo, reduced proteinuria and alleviated renal fibrosis without affecting hyperglycemia in DN rats. The potential mechanisms by which emodin exerts its renoprotective effects in vivo are through suppressing cell apoptosis and enhancing autophagy of podocytes via the AMPK/mTOR signaling pathway in the kidney.
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