ArticleScientific reports2016
KCa3.1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 79 citations in OpenAlex.
- Cell-state- and compartment-dependent PI3K/Akt redox signaling in chronic kidney disease: mechanisms and translational implications.Frontiers in pharmacology · 2026Review
- PCSK9 Inhibitors: A Potential Priority Choice for Lipid Management in Patients with Diabetic Kidney Disease.Drugs · 2025Review
- Systems Biology of Human Microbiome for the Prediction of Personal Glycaemic Response.Diabetes & metabolism journal · 2024Review
- The key mediator of diabetic kidney disease: Potassium channel dysfunction.Genes & diseases · 2024Review
- Article
- Amifostine attenuates bleomycin-induced pulmonary fibrosis in mice through inhibition of the PI3K/Akt/mTOR signaling pathway.Scientific reports · 2023Article
- Role of renal tubular programed cell death in diabetic kidney disease.Diabetes/metabolism research and reviews · 2023Review
- KCa3.1 Promotes Proinflammatory Exosome Secretion by Activating AKT/Rab27a in Atrial Myocytes during Rapid Pacing.Cardiovascular therapeutics · 2023Article
- High-Glucose-Induced Injury to Proximal Tubules of the Renal System Is Alleviated by Netrin-1 Suppression of Akt/mTOR.Journal of diabetes research · 2023Article
- The Interaction of Food Allergy and Diabetes: Food Allergy Effects on Diabetic Mice by Intestinal Barrier Destruction and Glucagon-like Peptide 1 Reduction in Jejunum.Foods (Basel, Switzerland) · 2022Article
- Systematic characterization of the components and molecular mechanisms of Jinshui Huanxian granules using UPLC-Orbitrap Fusion MS integrated with network pharmacology.Scientific reports · 2022Article
- Profiling the lncRNA-miRNA-mRNA interaction network in the submandibular gland of diabetic mice.BMC endocrine disorders · 2022Article
- A single-domain i-body, AD-114, attenuates renal fibrosis through blockade of CXCR4.JCI insight · 2022Article
- Autophagy in renal fibrosis: Protection or promotion?Frontiers in pharmacology · 2022Review
- Mitochondria in Diabetic Kidney Disease.Cells · 2021Review
- Article
- Cardamonin exerts a protective effect against autophagy and apoptosis in the testicles of diabetic male rats through the expression of Nrf2The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Article
- KCa3.1 Mediates Dysregulation of Mitochondrial Quality Control in Diabetic Kidney Disease.Frontiers in cell and developmental biology · 2021Article
- Update on the Mechanisms of Tubular Cell Injury in Diabetic Kidney Disease.Frontiers in medicine · 2021Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is emerging as an important pathway in many diseases including diabetic nephropathy. It is acknowledged that oxidative stress plays a critical role in autophagy dysfunction and diabetic nephropathy, and KCa3.1 blockade ameliorates diabetic renal fibrosis through inhibiting TGF-β1 signaling pathway. To identify the role of KCa3.1 in dysfunctional tubular autophagy in diabetic nephropathy, human proximal tubular cells (HK2) transfected with scrambled or KCa3.1 siRNAs were exposed to TGF-β1 for 48 h, then autophagosome formation, the autophagy marker LC3, signaling molecules PI3K, Akt and mTOR, and oxidative stress marker nitrotyrosine were examined respectively. In vivo, LC3, nitrotyrosine and phosphorylated mTOR were examined in kidneys of diabetic KCa3.1+/+ and KCa3.1-/- mice. The results demonstrated that TGF-β1 increased the formation of autophagic vacuoles, LC3 expression, and phosphorylation of PI3K, Akt and mTOR in scrambled siRNA transfected HK2 cells compared to control cells, which was reversed in KCa3.1 siRNA transfected HK2 cells. In vivo, expression of LC3 and nitrotyrosine, and phosphorylation of mTOR were significantly increased in kidneys of diabetic KCa3.1+/+ mice compared to non-diabetic mice, which were attenuated in kidneys of diabetic KCa3.1-/- mice. These results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt/mTOR signaling pathways.
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