ArticleAntioxidants & redox signaling2016
mTORC2 Signaling Regulates Nox4-Induced Podocyte Depletion in Diabetes.
Article in Antioxidants & redox signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 66 citations in OpenAlex.
- The role of mTORC2/RICTOR in immune cells and inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Research Progress on Pathogenesis of Diabetic Nephropathy and Intervention with Traditional Chinese Medicine.Journal of multidisciplinary healthcare · 2026Review
- Pathogenic Role of mTOR Signaling in Cardiometabolic Disease: Implications for Heart, Liver, and Kidney Dysfunction.Physiological research · 2025Review
- Rictor/mTORC2 signalling contributes to renal vascular endothelial-to-mesenchymal transition and renal allograft interstitial fibrosis by regulating BNIP3-mediated mitophagy.Clinical and translational medicine · 2024Article
- Acteoside protects podocyte against apoptosis through regulating AKT/GSK-3β signaling pathway in db/db mice.BMC endocrine disorders · 2023Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- Unraveling the Crosstalk between Lipids and NADPH Oxidases in Diabetic Kidney Disease.Pharmaceutics · 2023Review
- SGLT2 Inhibitor-Dapagliflozin Attenuates Diabetes-Induced Renal Injury by Regulating Inflammation through a CYP4A/20-HETE Signaling Mechanism.Pharmaceutics · 2023Article
- Clinical application of RUBCN/SESN2 mediated inhibition of autophagy as biomarkers of diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2022Article
- In Vitro Photodynamic Treatment Modality for A375 Melanoma Cell Line Using a Sulphonated Aluminum Phthalocyanine Chloride-Photosensitizer-Gold Nanoparticle Conjugate.Pharmaceutics · 2022Article
- Intestinal microbiota regulates diabetes and cancer progression by IL-1β and NOX4 dependent signaling cascades.Cellular and molecular life sciences : CMLS · 2022Article
- Sestrin2 remedies podocyte injury via orchestrating TSP-1/TGF-β1/Smad3 axis in diabetic kidney disease.Cell death & disease · 2022Article
- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- Reno-Protective Effect of GLP-1 Receptor Agonists in Type1 Diabetes: Dual Action on TRPC6 and NADPH Oxidases.Biomedicines · 2021Article
- CYP450 Mediates Reactive Oxygen Species Production in a Mouse Model of β-Thalassemia through an Increase in 20-HETE Activity.International journal of molecular sciences · 2021Article
- COVID-19 and diabetes mellitus: how one pandemic worsens the other.Reviews in endocrine & metabolic disorders · 2020Review
- Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species.World journal of stem cells · 2020Review
- Modulation of radiation-induced damage of human glomerular endothelial cells by SMPDL3B.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Plant-Based Antidiabetic Nanoformulations: The Emerging Paradigm for Effective Therapy.International journal of molecular sciences · 2020Review
- Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
Abstract
aimPodocyte apoptosis is a critical mechanism for excessive loss of urinary albumin that eventuates in kidney fibrosis. Oxidative stress plays a critical role in hyperglycemia-induced glomerular injury. We explored the hypothesis that mammalian target of rapamycin complex 2 (mTORC2) mediates podocyte injury in diabetes.
resultsHigh glucose (HG)-induced podocyte injury reflected by alterations in the slit diaphragm protein podocin and podocyte depletion/apoptosis. This was paralleled by activation of the Rictor/mTORC2/Akt pathway. HG also increased the levels of Nox4 and NADPH oxidase activity. Inhibition of mTORC2 using small interfering RNA (siRNA)-targeting Rictor in vitro decreased HG-induced Nox1 and Nox4, NADPH oxidase activity, restored podocin levels, and reduced podocyte depletion/apoptosis. Inhibition of mTORC2 had no effect on mammalian target of rapamycin complex 1 (mTORC1) activation, described by our group to be increased in diabetes, suggesting that the mTORC2 activation by HG could mediate podocyte injury independently of mTORC1. In isolated glomeruli of OVE26 mice, there was a similar activation of the Rictor/mTORC2/Akt signaling pathway with increase in Nox4 and NADPH oxidase activity. Inhibition of mTORC2 using antisense oligonucleotides targeting Rictor restored podocin levels, reduced podocyte depletion/apoptosis, and attenuated glomerular injury and albuminuria. INNOVATION: Our data provide evidence for a novel function of mTORC2 in NADPH oxidase-derived reactive oxygen species generation and podocyte apoptosis that contributes to urinary albumin excretion in type 1 diabetes.
conclusionmTORC2 and/or NADPH oxidase inhibition may represent a therapeutic modality for diabetic kidney disease. Antioxid. Redox Signal. 25, 703-719.
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Registered trials
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 Socratic graph.