ArticleJournal of cellular physiology2011
Effects of insulin and high glucose on mobilization of slo1 BKCa channels in podocytes.
Article in Journal of cellular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- Extracellular Vesicles Facilitate the Crosstalk Between High Glucose-Stimulated Mesangial Cells and Healthy Podocytes to Mediate Injury Responses.International journal of molecular sciences · 2026Article
- Article
- The key mediator of diabetic kidney disease: Potassium channel dysfunction.Genes & diseases · 2024Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- The role of protein tyrosine phosphatase 1B (PTP1B) in the pathogenesis of type 2 diabetes mellitus and its complications.Journal of physiology and biochemistry · 2022Review
- GPR43 deficiency protects against podocyte insulin resistance in diabetic nephropathy through the restoration of AMPKα activity.Theranostics · 2021Article
- Expression of a Constitutively Active Human Insulin Receptor in Hippocampal Neurons Does Not Alter VGCC Currents.Neurochemical research · 2019Article
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- Mechanism of Regulation of Big-Conductance CaFrontiers in physiology · 2019Article
- The Evolving Importance of Insulin Signaling in Podocyte Health and Disease.Frontiers in endocrinology · 2018Review
- The metabolic syndrome and chronic kidney disease.Translational research : the journal of laboratory and clinical medicine · 2017Review
- The impact of insulin resistance on the kidney and vasculature.Nature reviews. Nephrology · 2016Review
- Large-Conductance Calcium-Activated Potassium Channels in Glomerulus: From Cell Signal Integration to Disease.Frontiers in physiology · 2016Review
- Selective Insulin Resistance in the Kidney.BioMed research international · 2016Review
- Obesity and renovascular disease.American journal of physiology. Renal physiology · 2015Review
- Paediatrics, insulin resistance and the kidney.Pediatric nephrology (Berlin, Germany) · 2015Review
- Insulin signaling: implications for podocyte biology in diabetic kidney disease.Current opinion in nephrology and hypertension · 2015Article
- The Ras GTPase-activating-like protein IQGAP1 is downregulated in human diabetic nephropathy and associated with ERK1/2 pathway activation.Molecular and cellular biochemistry · 2014Article
- Podocytes, signaling pathways, and vascular factors in diabetic kidney disease.Advances in chronic kidney disease · 2014Review
- ATP acting through P2Y receptors causes activation of podocyte TRPC6 channels: role of podocin and reactive oxygen species.American journal of physiology. Renal physiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Podocytes are dynamic polarized cells that lie on the surface of glomerular capillaries and comprise an essential component of the glomerular filtration barrier. Podocytes are affected in the earliest stages of diabetic nephropathy and insulin signaling to podocytes is essential for normal glomerular function. Large-conductance Ca(2+)-activated K(+) channels (BK(Ca) channels) encoded by the Slo1 gene are expressed in podocytes in a complex with multiple glomerular slit diaphragm proteins including nephrin, TRPC6 channels, and several different actin-binding proteins. Here we show that insulin increases cell surface expression of podocyte BK(Ca) channels, which is accompanied by a corresponding increase in the density of current flowing through these channels. Insulin stimulation of BK(Ca) channels was detectable in 15 min and required activation of both Erk and Akt signaling cascades. Exposure to high glucose (36.1 mM) for 24 h caused a marked reduction in the steady-state surface expression of BK(Ca) channels as well as of the slit diaphragm signaling molecule nephrin. High glucose treatment also abolished the stimulatory effects of insulin on BK(Ca) current density, although insulin continued to increase phosphorylation of Erk and Akt under those conditions. Therefore, in contrast to most other cell types, high glucose abrogates the effects of insulin in podocytes at relatively distal steps in its signaling pathway. Insulin stimulation of BK(Ca) channels in podocytes may prepare podocytes to adapt to changes in pressure gradients that occur during postprandial hyperfiltration.
Indexed as
Identifiers
What OpenQuestion holds
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.