ArticleAmerican journal of physiology. Renal physiology2019
Prompt apoptotic response to high glucose in SGLT-expressing renal cells.
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 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Mizagliflozin ameliorates diabetes induced kidney injury by inhibitor inhibit inflammation and oxidative stress.World journal of diabetes · 2025Article
- Tubulointerstitial injury in proteinuric chronic kidney diseases.Frontiers in medicine · 2024Review
- The Mitochondrion: A Promising Target for Kidney Disease.Pharmaceutics · 2023Review
- LncRNA H19: a novel player in the regulation of diabetic kidney disease.Frontiers in endocrinology · 2023Review
- The Na/K-ATPase Signaling and SGLT2 Inhibitor-Mediated Cardiorenal Protection: A Crossed Road?The Journal of membrane biology · 2021Review
- Super-resolution microscopy reveals that NaCell death & disease · 2021Article
- Current Challenges and Future Perspectives of Renal Tubular Dysfunction in Diabetic Kidney Disease.Frontiers in endocrinology · 2021Review
- Molecular Mechanisms of SGLT2 Inhibitor on Cardiorenal Protection.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is generally believed that cells that are unable to downregulate glucose transport are particularly vulnerable to hyperglycemia. Yet, little is known about the relation between expression of glucose transporters and acute toxic effects of high glucose exposure. In the present ex vivo study of rat renal cells, we compared the apoptotic response to a moderate increase in glucose concentration. We studied cell types that commonly are targeted in diabetic kidney disease (DKD): proximal tubule cells, which express Na
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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.