ArticleFrontiers in endocrinology2018
Angiotensin II Modulates Podocyte Glucose Transport.
Article in Frontiers in endocrinology, 2018. 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, 12 citations in OpenAlex.
- Emerging roles of cannabinoid pathways in renal injury and repair.Frontiers in pharmacology · 2026Review
- Modulation of podocyte extracellular matrix remodeling in membranous nephropathy by the NFATc3/LRRC55/BK channel pathway.Journal of cell communication and signaling · 2025Article
- G protein-coupled receptor 107 deficiency promotes development of diabetic nephropathy.Molecular biomedicine · 2025Article
- Research on podocyte injury mechanisms in diabetic nephropathy: a bibliometric and knowledge-map analysis from 2000 to 2024.Frontiers in endocrinology · 2025Article
- One Molecule for Mental Nourishment and More: Glucose Transporter Type 1-Biology and Deficiency Syndrome.Biomedicines · 2022Review
- Human Glucose Transporters in Renal Glucose Homeostasis.International journal of molecular sciences · 2021Review
- Losartan Protects Podocytes against High Glucose-induced Injury by Inhibiting B7-1 Expression.Current medical science · 2021Article
- Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury.Molecular medicine reports · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocytes play a central role in the maintenance of the glomerular filtration barrier and are cellular targets of angiotensin II (AngII). Non-hemodynamic pathways of AngII signaling regulate cellular function and mediate podocyte abnormalities that are associated with various glomerulopathies, including diabetic kidney disease. In this study we investigated the capacity of AngII to modulate glucose uptake in mouse podocytes expressing the human AT1 receptor (AT1R+) after 5 days of exposure to normal (NG, 5.6 mmol/L) or to high (HG, 30 mmol/L) glucose. Short (30 min) as well as long-term (24 h) incubations with AngII markedly enhanced glucose transport in both NG and HG cells. In podocytes cultured under NG conditions, AngII inhibited insulin-stimulated glucose uptake. Regardless of the presence or absence of AngII, no effect of insulin on glucose uptake was observed in HG cells. Stimulation of glucose transport by AngII was mediated by protein kinase C and by phosphoinositide 3
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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.