ArticleProceedings of the National Academy of Sciences of the United States of America2000
Deranged transcriptional regulation of cell-volume-sensitive kinase hSGK in diabetic nephropathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed.
- Unraveling the Potential of SGK1 in Osteoporosis: From Molecular Mechanisms to Therapeutic Targets.Biomolecules · 2025Review
- Intrauterine hyperglycemia impairs endometrial receptivity via up-regulating SGK1 in diabetes.Science China. Life sciences · 2022Article
- Does the early aldosterone-induced SGK1 play a role in early Kaliuresis?Physiological reports · 2022Article
- Serum and Glucocorticoid-Inducible Kinase 1 (SGK1) in NSCLC Therapy.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Role of SGK1 in the Osteogenic Transdifferentiation and Calcification of Vascular Smooth Muscle Cells Promoted by Hyperglycemic Conditions.International journal of molecular sciences · 2020Article
- SGK1 mediates the hypotonic protective effect against HActa pharmacologica Sinica · 2020Article
- Renal Effects of Fetal Reprogramming With Pentaerythritol Tetranitrate in Spontaneously Hypertensive Rats.Frontiers in pharmacology · 2020Article
- The impact of insulin resistance on the kidney and vasculature.Nature reviews. Nephrology · 2016Review
- Sodium glucose cotransporter SGLT1 as a therapeutic target in diabetes mellitus.Expert opinion on therapeutic targets · 2016Review
- Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis.International journal of molecular sciences · 2016Review
- Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway.Clinical and experimental nephrology · 2015Article
- Sodium chloride, SGK1, and Th17 activation.Pflugers Archiv : European journal of physiology · 2015Review
- Disturbance of oligodendrocyte function plays a key role in the pathogenesis of schizophrenia and major depressive disorder.BioMed research international · 2015Review
- Diverse effects of ANXA7 and p53 on LNCaP prostate cancer cells are associated with regulation of SGK1 transcription and phosphorylation of the SGK1 target FOXO3A.BioMed research international · 2014Article
- Aldosterone stimulates nuclear factor-kappa B activity and transcription of intercellular adhesion molecule-1 and connective tissue growth factor in rat mesangial cells via serum- and glucocorticoid-inducible protein kinase-1.Clinical and experimental nephrology · 2012Review
- Serum- and glucocorticoid-inducible kinase 1 in the regulation of renal and extrarenal potassium transport.Clinical and experimental nephrology · 2012Review
- Angiotensin II mediates cell survival through upregulation and activation of the serum and glucocorticoid inducible kinase 1.Cellular signalling · 2012Article
- Transcription factor NF-κB regulates expression of pore-forming Ca2+ channel unit, Orai1, and its activator, STIM1, to control Ca2+ entry and affect cellular functions.The Journal of biological chemistry · 2012Article
- Functional expression of TRPV4 channels in human collecting duct cells: implications for secondary hypertension in diabetic nephropathy.Experimental diabetes research · 2012Article
- Pathophysiology of the diabetic kidney.Comprehensive Physiology · 2011Review
Corrections and comments
- Commented on by
Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor beta (TGF-beta) has been shown to participate in the pathophysiology of diabetic complications. As shown most recently, TGF-beta stimulates the expression of a distinct serine/threonine kinase (hSGK) which had previously been cloned as an early gene transcriptionally regulated by cell volume alterations. The present study was performed to elucidate transcription and function of hSGK in diabetic nephropathy. As shown by Northern blotting, an increase of extracellular glucose concentration increased hSGK mRNA levels in cultured cells, an effect qualitatively mimicked by osmotic cell shrinkage or treatment with TGF-beta (2 microgram/liter), phorbol 12,13-didecanoate (1 microM), or the Ca(2+) ionophore ionomycin (1 microM) and blunted by high concentrations of nifedipine (10 and 100 microM). In situ hybridization revealed that hSGK transcription was markedly enhanced in diabetic nephropathy, with particularly high expression in mesangial cells, interstitial cells, and cells in thick ascending limbs of Henle's loop and distal tubules. According to voltage clamp and tracer flux studies in Xenopus oocytes expressing the renal epithelial Na(+) channel ENaC or the mouse thick ascending limb Na(+),K(+),2Cl(-) cotransporter BSC-1, coexpression with hSGK stimulated ENaC and BSC-1 11-fold and 6-fold, respectively, effects reversed by kinase inhibitors staurosporine (1 microM) and chelerythrine (1 microM) and not elicited by inactive hSGK. In conclusion, excessive extracellular glucose concentrations enhance hSGK transcription, which in turn stimulates renal tubular Na(+) transport. These observations disclose an additional element in the pathophysiology of diabetic nephropathy.
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.