ArticleFrontiers in endocrinology2022
TangShenWeiNing Formula Prevents Diabetic Nephropathy by Protecting Podocytes Through the SIRT1/HIF-1α Pathway.
Article in Frontiers in endocrinology, 2022. 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, 19 citations in OpenAlex.
- The mechanism and therapeutic prospect of HIF-1 α/BNIP3 pathway in regulating mitophagy in tubulointerstitial fibrosis.Renal failure · 2026Review
- Investigation of Protective Effects of Carvacrol and Hesperidin in Rats with Streptozotocin-Induced Diabetic Nephropathy.Life (Basel, Switzerland) · 2026Article
- The translational potential of m6A RNA methylation in DKD: emerging biomarkers for early detection and targeted therapies.Frontiers in medicine · 2026Review
- Traditional Chinese medicine in the treatment of diabetic kidney disease: the mechanisms of signaling pathways regulations.Frontiers in endocrinology · 2026Review
- TangShenWeiNing formula alleviates diabetic kidney disease by inhibiting ferroptosis via AMPK pathway in renal tubular epithelial cells.Frontiers in endocrinology · 2026Article
- Icariside II inhibits ferroptosis and improves high-glucose-induced podocytes injury by downregulating DNMT1.In vitro cellular & developmental biology. Animal · 2026Article
- Astragalus polysaccharide alleviates diabetic nephropathy via SIRT1-dependent activation of FOXO3a/BNIP3 pathway to enhance podocyte autophagy.Scientific reports · 2025Article
- Single-cell transcriptome analysis highlights a critical role of ATG5 for endothelial cells in diabetic nephropathy.Human cell · 2025Article
- Yiqi Yangyin Tongluo prescription targets lncRNA VIM-AS1 to regulate FOXK2/mTOR to promote autophagy and inhibit renal tubular epithelial cell apoptosis.Journal of food and drug analysis · 2025Article
- The effect and mechanism of freeze-dried powder ofHeliyon · 2024Article
- Effects of xenogeneic transplantation of umbilical cord-derived mesenchymal stem cells combined with irbesartan on renal podocyte damage in diabetic rats.Stem cell research & therapy · 2024Article
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- Jian-Pi-Gu-Shen-Hua-Yu Decoction Alleviated Diabetic Nephropathy in Mice through Reducing Ferroptosis.Journal of diabetes research · 2024Article
- Common mechanisms underlying diabetic vascular complications: focus on the interaction of metabolic disorders, immuno-inflammation, and endothelial dysfunction.Cell communication and signaling : CCS · 2023Review
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Diabetic nephropathy (DN) represents a major complication of diabetes, and podocyte injury has a critical function in DN development. TangShenWeiNing formula (TSWN) has been demonstrated to efficiently decrease proteinuria and protect podocytes in DN. This work aimed to explore the mechanism by which TSWN alleviates DN and protects podocytes. Methods: The major bioactive components of TSWN were detected by mass spectrometry (MS) and pharmacological databases. Eight-week-old male C57BLKS/J db/m and db/db mice were provided pure water, valsartan, low dose TSWN, middle dose TSWN and high dose TSWN by gavage for 12 weeks, respectively. Results: MS and network pharmacology analyses suggested that TSWN might prevent DN through the sirtuin (SIRT)1/hypoxia-inducible factor (HIF)-1α pathway. Diabetic mice showed elevated urinary albumin in comparison with non-diabetic mice, and TSWN decreased urinary albumin in diabetic mice. Histological injury increased in the kidney in diabetic mice, which could be improved by TSWN. Fibrosis and collagen I expression were induced in the diabetic mouse kidney in comparison with the non-diabetic mouse kidney; TSWN alleviated these effects. Apoptosis and cleaved caspase-3 were induced in the diabetic mouse kidney in comparison with the non-diabetic mouse kidney, and TSWN blunted these effects. Podocytes were damaged in the diabetic mouse kidney, which was improved by TSWN. Podocin and nephrin amounts were decreased in the diabetic mouse kidney in comparison with the non-diabetic mouse kidney, and podocalyxin was increased in urine of diabetic animals in comparison with non-diabetic counterparts. After TSWN treatment, podocin and nephrin were raised in the diabetic mouse kidney, and urinary podocalyxin was depressed in diabetic animals. Diabetic mice had lower SIRT1 and higher HIF-1α amounts in kidney specimens in comparison with non-diabetic mice, and TSWN promoted SIRT1 and inhibited HIF-1α in the diabetic mouse kidney. Moreover, co-staining of SIRT1 and podocin revealed that SIRT1 decreased in podocytes from diabetic mice in comparison with those from non-diabetic mice, and TSWN elevated SIRT1 in podocytes. Conclusions: This study indicated that TSWN alleviates DN by improving podocyte injury through the SIRT1/HIF-1α pathway in diabetic mouse kidneys.
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