ArticleRedox biology2020
Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 91 citations in OpenAlex.
- Protective Effects and Mechanisms of Extracellular Vesicles in Remote Ischemic Preconditioning on Renal Injury Induced by Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Construction of an activatable ratiometric fluorescent nanoprobe for HClO detection and imaging in acute kidney injury models.RSC advances · 2026Article
- Urinary microenvironment-degradable nanocapsules for traceable therapy of diabetic nephropathy.Materials today. Bio · 2026Article
- TGFβ-activated PDHB promotes mitochondrial pyruvate metabolism and contributes to human endoderm differentiation via ATP-dependent BRG1.Nature communications · 2026Article
- SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Annexin A13 Protects Against Acute Kidney Injury by Inactivating TGF-β/Smad3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- From Defense to Disease: NADPH Oxidase in Cellular Function and Dysregulation.Journal of immunology research · 2026Review
- Butyrate mitigates multi-organ damage in urosepsis: associated changes in the renal NOX4/ROS/NF-κB axis and gut microbiota.Frontiers in cellular and infection microbiology · 2026Article
- Targeting tubular NAT10 ameliorates the renal Tubulointerstitial Fibrosis in Obstructive and Folic Acid-Induced Nephropathy.International journal of biological sciences · 2026Article
- Triptolide improves microbial dysbiosis and metabolite disorder in db/db mice.Renal failure · 2025Article
- Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular Basis of Oxidative Stress-Induced Acute Kidney Injury, Kidney Fibrosis, Chronic Kidney Disease, and Clinical Significance of Targeting Reactive Oxygen Species-Regulated Pathways to Treat Kidney Disease.Frontiers in bioscience (Scholar edition) · 2025Review
- Genetic and Pharmacological Inhibition of NOX4 Protects Against Rhabdomyolysis-Induced Acute Kidney Injury Through Suppression of Endoplasmic Reticulum Stress.Antioxidants (Basel, Switzerland) · 2025Article
- PARylation promotes acute kidney injuryActa pharmaceutica Sinica. B · 2025Article
- C5a-Induced Autophagy Dysfunction Promotes Choroidal Neovascularization Through the ROS-Inflammatory Pathway.Investigative ophthalmology & visual science · 2025Article
- Reduced glutathione enhances adipose tissue-derived mesenchymal stem cell engraftment efficiency for liver fibrosis by targeting TGFβ1/SMAD3/NOX4 pathway.Bioengineering & translational medicine · 2025Article
- Hypericin Nanoparticles-Associated Photodynamic Therapy Modulates the Biological Behavior of Hepatocellular Carcinoma by SERPINE1.International journal of nanomedicine · 2025Article
- Plant-inspired visible-light-driven bioenergetic hydrogels for chronic wound healing.Bioactive materials · 2024Article
- Advanced glycation end products and reactive oxygen species: uncovering the potential role of ferroptosis in diabetic complications.Molecular medicine (Cambridge, Mass.) · 2024Review
- TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review).Molecular medicine reports · 2024Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence and severity of acute kidney injury (AKI) is increased yearly in diabetic patients. Although the mechanisms for this remain unclear, the prevention of AKI in diabetic nephropathy is feasible and of value. As we detected highly activation of TGF-β/Smad3 signaling in both human biopsy and mouse model of diabetic nephropathy, we hypothesized that Smad3 activation in diabetic kidneys may increase AKI sensitivity. We tested our hypothesis in vitro using TGF-β type II receptor (TGF-βRII) disrupted tubular epithelial cells (TECs) and in vivo in mice with streptozotocin (STZ)-induced diabetic nephropathy before the induction of ischemia/reperfusion (I/R) injury. We found that high glucose (HG)-cultured TECs showed increased inflammation, apoptosis and oxidative stress following hypoxia/reoxygenation (H/R) injury. Disruption of TGF-βRII attenuated cell injury induced by H/R in HG-treated TECs. Consistently, Smad3 knockdown in diabetic kidney attenuated I/R-induced AKI. Mechanistically, Smad3 binds to p53 and enhances p53 activity in cells treated with HG and H/R, which may lead to TECs apoptosis. Additionally, ChIP assay showed that Smad3 bound with the promoter region of NOX4 and induced ROS production and inflammation. In conclusion, our results demonstrate that Smad3 promotes AKI susceptibility in diabetic mice by interacting with p53 and NOX4.
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Registered trials
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