ArticleProceedings of the National Academy of Sciences of the United States of America2015
Low TGFβ1 expression prevents and high expression exacerbates diabetic nephropathy in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 95 citations in OpenAlex.
- Cyanoglycosides isolated fromPharmaceutical biology · 2026Article
- PLCε regulates podocyte differentiation and TGF-β1 responses via alteration of SMAD2/SMAD3 ratio.Cell communication and signaling : CCS · 2026Article
- Inhibition of cell surface GRP78 and activated α2M interaction attenuates kidney fibrosis.JCI insight · 2025Article
- miR-299a-5p is a mediator of fibrosis in diabetic kidney disease by regulating follistatin and cripto-1.Communications biology · 2025Article
- Proximal aortic aneurysms in mice underexpressing transforming growth factor-β1.The journal of physiological sciences : JPS · 2025Article
- Targeting programmed cell death pathways: emerging therapeutic strategies for diabetic kidney disease.Frontiers in endocrinology · 2025Review
- Modulation of TGF-β signaling new approaches toward kidney disease and fibrosis therapy.International journal of biological sciences · 2025Review
- Elucidating the Differential Mechanisms of Jingui Shenqi Pill and Mingmu Dihuang Pill in the Treatment of Diabetic Nephropathy Based on Yin-Yang Theory.Drug design, development and therapy · 2025Article
- Transcriptomics and Proteomics Reveal That TLPW Acupuncture Ameliorates Proteinuria in Diabetic Kidney Disease Model Rats by Suppressing Epithelial-to-Mesenchymal Transition via the DPP4/SDF-1Journal of diabetes research · 2025Article
- LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Picroside Ⅱ alleviates renal fibrosis through YY1-dependent transcriptional inhibition of TGFβ1.Metabolism open · 2024Article
- Sleeve gastrectomy links the attenuation of diabetic kidney disease to the inhibition of renal tubular ferroptosis through down-regulating TGF-β1/Smad3 signaling pathway.Journal of endocrinological investigation · 2024Article
- Article
- Circulating exosomal miR-16-5p and let-7e-5p are associated with bladder fibrosis of diabetic cystopathy.Scientific reports · 2024Article
- Exploring unconventional targets in myofibroblast transdifferentiation outside classical TGF-Frontiers in physiology · 2024Review
- Association between serum vitamin D and the risk of diabetic kidney disease in patients with type 2 diabetes.Frontiers in medicine · 2024Article
- Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023Review
- The miR-143/145 cluster induced by TGF-β1 suppresses Wilms' tumor 1 expression in cultured human podocytes.American journal of physiology. Renal physiology · 2023Article
- A therapeutic target for CKD: activin A facilitates TGFβ1 profibrotic signaling.Cellular & molecular biology letters · 2023Article
- Jiangtang Decoction Ameliorates Diabetic Kidney Disease Through the Modulation of the Gut Microbiota.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Nephropathy develops in many but not all patients with long-standing type 1 diabetes. Substantial efforts to identify genotypic differences explaining this differential susceptibility have been made, with limited success. Here, we show that the expression of the transforming growth factor β1 gene (Tgfb1) affects the development of diabetic nephropathy in mice. To do this we genetically varied Tgfb1 expression in five steps, 10%, 60%, 100%, 150%, and 300% of normal, in mice with type 1 diabetes caused by the Akita mutation in the insulin gene (Ins2(Akita)). Although plasma glucose levels were not affected by Tgfb1 genotype, many features of diabetic nephropathy (mesangial expansion, elevated plasma creatinine and urea, decreased creatinine clearance and albuminuria) were progressively ameliorated as Tgfb1 expression decreased and were progressively exacerbated when expression was increased. The diabetic 10% hypomorphs had comparable creatinine clearance and albumin excretion to wild-type mice and no harmful changes in renal morphology. The diabetic 300% hypermorphs had ∼1/3 the creatinine clearance of wild-type mice, >20× their albumin excretion, ∼3× thicker glomerular basement membranes and severe podocyte effacement, matching human diabetic nephropathy. Switching Tgfb1 expression from low to high in the tubules of the hypomorphs increased their albumin excretion more than 10-fold but creatinine clearance remained high. Switching Tgfb1 expression from low to high in the podocytes markedly decreased creatinine clearance, but minimally increased albumin excretion. Decreasing expression of Tgfb1 could be a promising option for preventing loss of renal function in diabetes.
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