ArticleInternational journal of biological sciences2021
Latent TGF-β1 protects against diabetic kidney disease via Arkadia/Smad7 signaling.
Article in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- TGF-β/Smad Signaling Pathway in Tubulointerstitial Fibrosis.Frontiers in pharmacology · 2022Pooled it
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Retinol saturase promotes tubulointerstitial fibrosis in diabetic kidney disease by inhibiting ChREBP ubiquitination via Smurf2 suppression.Frontiers in endocrinology · 2026Article
- TGF-β in chronic kidney disease: a controversy for decades.Frontiers in immunology · 2026Review
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- TGF-β: elusive target in diabetic kidney disease.Renal failure · 2025Review
- Review
- FOSL2 activates TGF-β1-mediated GLUT1/mTOR signaling to promote diabetic kidney disease.Journal of diabetes investigation · 2025Article
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Editorial: Cell cross-talk in diabetic kidney diseases, volume III.Frontiers in medicine · 2025Article
- The Renal Micro-Vasculopathy and Systemic Aldosterone-Renin Ratio (ARR) in Type 2 Diabetic Patients-A Retrospective Real-World Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Adjunctive effects of intermittent fasting and exercise with glibenclamide on diabetic nephropathy in rats: a potential role of the polyol pathway.Frontiers in physiology · 2025Article
- TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review).Molecular medicine reports · 2024Review
- VDR restores the expression of PINK1 and BNIP3 in TECs of streptozotocin-induced diabetic mice.Life science alliance · 2024Article
- Treatment for type 2 diabetes and diabetic nephropathy by targeting Smad3 signaling.International journal of biological sciences · 2024Article
- Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024Review
- Review
- [The Role of TGF-β1/SMAD in Diabetic Nephropathy: Mechanisms and Research Development].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Article
- Association between Usual Dietary Intake of Food Groups and DNA Methylation and Effect Modification by Metabotype in the KORA FF4 Cohort.Life (Basel, Switzerland) · 2022Article
- Article
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TGF-β1 has long been considered as a key mediator in diabetic kidney disease (DKD) but anti-TGF-β1 treatment fails clinically, suggesting a diverse role for TGF-β1 in DKD. In the present study, we examined a novel hypothesis that latent TGF-β1 may be protective in DKD mice overexpressing human latent TGF-β1. Streptozotocin-induced Type 1 diabetes was induced in latent TGF-β1 transgenic (Tg) and wild-type (WT) mice. Surprisingly, compared to WT diabetic mice, mice overexpressing latent TGF-β1 were protected from the development of DKD as demonstrated by lowing microalbuminuria and inhibiting renal fibrosis and inflammation, although blood glucose levels were not altered. Mechanistically, the renal protective effects of latent TGF-β1 on DKD were associated with inactivation of both TGF-β/Smad and nuclear factor-κB (NF-κB) signaling pathways. These protective effects were associated with the prevention of renal Smad7 from the Arkadia-induced ubiquitin proteasomal degradation in the diabetic kidney, suggesting protection of renal Smad7 from Arkadia-mediated degradation may be a key mechanism through which latent TGF-β1 inhibits DKD. This was further confirmed
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.