ArticleThe Journal of clinical investigation2013
Ubiquitylation and the pathogenesis of hypertension.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK.The Journal of physiology · 2025Article
- Mineralocorticoid receptor antagonists promote renal immunosenescence.International urology and nephrology · 2025Review
- Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension.International journal of molecular sciences · 2024Article
- Urine Cell Transcriptomes Implicate Specific Renal Inflammatory Pathways Associated With Difficult-to-Control Hypertension.Journal of the American Heart Association · 2023Article
- Ubiquitination of NKCC2 by the cullin-RING E3 ubiquitin ligase family in the thick ascending limb of the loop of Henle.American journal of physiology. Renal physiology · 2023Article
- Interleukin 17A: Key Player in the Pathogenesis of Hypertension and a Potential Therapeutic Target.Current hypertension reports · 2021Review
- MgAmerican journal of physiology. Renal physiology · 2019Article
- High Salt Activates CD11cHypertension (Dallas, Tex. : 1979) · 2019Article
- Renal Tubular Ubiquitin-Protein Ligase NEDD4-2 Is Required for Renal Adaptation during Long-Term Potassium Depletion.Journal of the American Society of Nephrology : JASN · 2017Article
- A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage.JCI insight · 2017Article
- Prevalence of Liddle Syndrome Among Young Hypertension Patients of Undetermined Cause in a Chinese Population.Journal of clinical hypertension (Greenwich, Conn.) · 2015Article
- Evaluation of the relationship between T663A polymorphism in the alpha-epithelial sodium channel gene and essential hypertension.Saudi medical journal · 2015Review
- Identifiable hypertension: a new spectrum.Journal of clinical hypertension (Greenwich, Conn.) · 2013Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Liddle syndrome is monogenic hypertension caused by mutations in the epithelial Na+ channel (ENaC) that interfere with its ubiquitylation by Nedd4-2. In this issue, Ronzaud and colleagues found that deleting Nedd4-2 from kidney tubules in adult mice led to ENaC accumulation, but not at the plasma membrane, as predicted from current models. Instead, abundance of the sodium chloride transporter NCC increased at the plasma membrane, and the mice have some features of increased NCC activity. Together, the results suggest that defective ubiquitylation of ENaC by Nedd4-2 may not fully explain Liddle syndrome and that Nedd4-2 modulates NCC more strongly.
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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.