ArticleCell death & disease2022
Sestrin2 remedies podocyte injury via orchestrating TSP-1/TGF-β1/Smad3 axis in diabetic kidney disease.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Review
- Development of an explainable machine learning model for predicting the occurrence of advanced diabetic kidney disease.Frontiers in endocrinology · 2026Article
- Mechanistic Insights and Therapeutic Advances of Anti-Inflammatory Biologics in Immune-Mediated Glomerulonephritis: A Narrative Review.Journal of inflammation research · 2026Review
- Microglial Sestrin2 alleviates depressive-like behaviors and cognitive impairment in a YTHDF1-dependent manner.Frontiers in neuroscience · 2026Article
- SLC11A1 can activate TGF-β1 signaling pathway to resist ferroptosis in colorectal cancer.Scientific reports · 2025Article
- TGF-β: elusive target in diabetic kidney disease.Renal failure · 2025Review
- Sestrin2 ameliorates LPS-induced cardiomyocyte injury by inhibiting ferroptosis via the Nrf2/HO-1 pathway.European journal of medical research · 2025Article
- SESN2 maintains cartilage homeostasis by SREBP1-mediated lipid metabolism during osteoarthritis progression.iScience · 2025Article
- SMAD3 orchestrates RNF167 and STAMBPL1-mediated Sestrin2 ubiquitination to drive gastric cancer progression.Cell division · 2025Article
- Blocking TSP1 Ameliorates Diabetes Mellitus-Induced Erectile Dysfunction by Inhibiting the TGF-β/SMAD Pathway.The world journal of men's health · 2025Article
- Mitigation of Ferroptosis in Diabetic Kidney Disease Through Mesenchymal Stem Cell Intervention via the Smad2/3/METTL3/S1PR1 Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Transcriptional Intermediary Factor 1γ-Induced Irisin in Skeletal Muscle Attenuates Renal Fibrosis in Diabetic Nephropathy.Journal of cachexia, sarcopenia and muscle · 2025Article
- Yishen Tongluo formula ameliorates kidney injury modulating inflammation and apoptosis in streptozotocin-induced diabetic kidney disease mice.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- METTL3 Potentiates M2 Macrophage-Driven MMT to Aggravate Renal Allograft Fibrosis via the TGF-β1/Smad3 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Diagnostic value of serum TGF-β1 and CysC in type 2 diabetic kidney disease: a cross-sectional study.Frontiers in medicine · 2025Article
- Targeting programmed cell death pathways: emerging therapeutic strategies for diabetic kidney disease.Frontiers in endocrinology · 2025Review
- Mir-615-3p promotes osteosarcoma progression via the SESN2/AMPK/mTOR pathway.Cancer cell international · 2024Article
- Enhancing Skin Wound Healing in Diabetic Mice Using SIKVAV-Modified Chitosan Hydrogels.Molecules (Basel, Switzerland) · 2024Article
- SETDB1 targeting SESN2 regulates mitochondrial damage and oxidative stress in renal ischemia-reperfusion injury.BMC biology · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sestrin2 is identified as a stress-induced protein and could functionate in many aspects. In our study, we investigated the latent impact of Sestrin2 on podocyte injury and its molecular mechanism in vivo and in vitro in diabetic kidney disease (DKD). Sestrin2 was low-expressed in renal biopsies from individuals with DKD, the glomeruli from diabetic mice, and mouse podocytes exposed to high glucose (HG). Sestrin2 overexpression ameliorated HG-induced phenotypic alterations, apoptosis, and oxidative stress in conditionally immortalized mouse podocytes and modulated the activity of Thrombospondin-1 (TSP-1)/transforming growth factor (TGF-β1)/Smad3 pathway in podocytes. Moreover, TSP-1 inhibitor LSKL or TGF-β blocker Pirfenidone arrested podocyte injury induced by HG. Streptozotocin (STZ) was employed to render equivalent diabetes in B6-TgN (CMV-Sestrin2) (TgN) and wild-type (WT) control mice. Sestrin2 alleviated increased levels of 24-h urinary protein, blood urea nitrogen, serum creatinine and triglyceride, and urine 8-OHdG in diabetic mice. Podocyte phenotypic alterations, increased expression of apoptosis-associated proteins and podocyte loss were observed in WT but not in diabetic TgN mice, as well as oxidative stress. Additionally, TSP-1/TGF-β1/Smad3 signaling pathway was also suppressed in glomeruli of diabetic TgN mice. Thus, Sestrin2 mitigates podocyte injury in DKD via orchestrating TSP-1/TGF-β1/Smad3 pathway, underlining Sestrin2 as a promising therapeutic target for DKD.
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