ArticleAntioxidants (Basel, Switzerland)2021
Roles of mTOR in Diabetic Kidney Disease.
Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Aging-driven transcriptional programs in diabetic kidney disease: multi-omics discovery of diagnostic biomarkers and drug-repurposing targets.Clinical epigenetics · 2026Article
- Yiqi Huoxue Yangyin Decoction Ameliorates Diabetic Nephropathy by Targeting AMPK/mTOR-Mediated Autophagy: A Network Pharmacology-Guided in vivo and in vitro Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- NMR metabolomics in genetically engineered mouse models.Biophysical reviews · 2025Review
- Adenosine Monophosphate-Activated Protein Kinase Activation and Mammalian Target of Rapamycin Complex 1 Inhibition: A Mechanistic Rationale for Anti-Aging Therapy in Type 2 Diabetes.Journal of clinical medicine research · 2025Review
- Potential Role of SGLT-2 Inhibitors in Improving Allograft Function and Reducing Rejection in Kidney Transplantation.Clinical transplantation · 2025Review
- The TXNIP-mTOR-Autophagy axis in diabetic kidney disease: mechanistic insights and therapeutic implications.Molecular biology reports · 2025Review
- Machine learning-based stratification of prediabetes and type 2 diabetes progression.Diabetology & metabolic syndrome · 2025Article
- Extracellular vesicles derived from mesenchymal stem cells alleviate renal fibrosis via the miR-99b-5p/mTOR/autophagy axis in diabetic kidney disease.Stem cell research & therapy · 2025Article
- mTOR-Mediated Autophagy Regulates Cadmium-Induced Kidney Injury via Pyroptosis.International journal of molecular sciences · 2025Article
- Hyperosmotic Stress Promotes the Nuclear Translocation of TFEB in Tubular Epithelial Cells Depending on Intracellular CaCellular and molecular bioengineering · 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
- The Role of Sirtuins in Diabetic Nephropathy: A Comprehensive Review.Current protein & peptide science · 2025Review
- mTOR-mediated nutrient sensing and oxidative stress pathways regulate autophagy: a key mechanism for traditional Chinese medicine to improve diabetic kidney disease.Frontiers in pharmacology · 2025Review
- TXNIP deficiency attenuates renal fibrosis by modulating mTORC1/TFEB-mediated autophagy in diabetic kidney disease.Renal failure · 2024Article
- The overexpression of human amylin in pancreatic β cells facilitate the appearance of amylin aggregates in the kidney contributing to diabetic nephropathy.Scientific reports · 2024Article
- Female Protection Against Diabetic Kidney Disease Is Regulated by Kidney-Specific AMPK Activity.Diabetes · 2024Article
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Dihydroxyacetone phosphate accumulation leads to podocyte pyroptosis in diabetic kidney disease.Journal of cellular and molecular medicine · 2024Article
- Exercise as a therapeutic approach to alleviate diabetic kidney disease: mechanisms, clinical evidence and potential exercise prescriptions.Frontiers in medicine · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease and the number of patients affected is increasing worldwide. Thus, there is a need to establish a new treatment for DKD to improve the renal prognosis of diabetic patients. Recently, it has shown that intracellular metabolic abnormalities are involved in the pathogenesis of DKD. In particular, the activity of mechanistic target of rapamycin complex 1 (mTORC1), a nutrient-sensing signaling molecule, is hyperactivated in various organs of diabetic patients, which suggests the involvement of excessive mTORC1 activation in the pathogenesis of diabetes. In DKD, hyperactivated mTORC1 may be involved in the pathogenesis of podocyte damage, which causes proteinuria, and tubular cell injury that decreases renal function. Therefore, elucidating the role of mTORC1 in DKD and developing new therapeutic agents that suppress mTORC1 hyperactivity may shed new light on DKD treatments in the future.
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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 OpenQuestion graph.