ArticleAmerican journal of physiology. Renal physiology2019
High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6.
Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Downregulating lncRNA MIAT attenuates apoptosis of podocytes exposed to high glucose.Acta diabetologica · 2024Article
- The Mechanism of Hyperglycemia-Induced Renal Cell Injury in Diabetic Nephropathy Disease: An Update.Life (Basel, Switzerland) · 2023Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Article
- Enhanced Orai1-mediated store-operated CaThe Journal of biological chemistry · 2022Article
- Transient receptor potential cation channel 6 contributes to kidney injury induced by diabetes and hypertension.American journal of physiology. Renal physiology · 2022Article
- FOXA1 Suppresses SATB1 Transcription and Inactivates the Wnt/β-Catenin Pathway to Alleviate Diabetic Nephropathy in a Mouse Model.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Tacrolimus Protects Podocytes from Apoptosis via Downregulation of TRPC6 in Diabetic Nephropathy.Journal of diabetes research · 2021Article
- Role of opioid signaling in kidney damage during the development of salt-induced hypertension.Life science alliance · 2020Article
- Low-glucose-sensitive TRPC6 dysfunction drives hypoglycemia-induced cognitive impairment in diabetes.Clinical and translational medicine · 2020Article
- The Rab-Rabphilin system in injured human podocytes stressed by glucose overload and angiotensin II.American journal of physiology. Renal physiology · 2020Article
- Review
- TRPC Channels in Proteinuric Kidney Diseases.Cells · 2019Review
- Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. Gain of TRPC6 function and loss of podocin function induce podocyte injury. We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. The decreased podocin was diminished in TRPC6 knockdown podocytes. High glucose elevated intracellular Ca
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Registered trials
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