ArticleAmerican journal of physiology. Renal physiology2016
The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- From Ion Channels to Blood Pressure: Genetic Disorders of Renal Tubular Transport.Electrolyte & blood pressure : E & BP · 2026Review
- Potassium Effects on NCC Are Attenuated during Inhibition of Cullin E3-Ubiquitin Ligases.Cells · 2021Article
- WNK-SPAK/OSR1-NCC kinase signaling pathway as a novel target for the treatment of salt-sensitive hypertension.Acta pharmacologica Sinica · 2021Review
- Review
- Recent insights into sodium and potassium handling by the aldosterone-sensitive distal nephron: implications on pathophysiology and drug discovery.Journal of nephrology · 2020Review
- Weighted gene co-expression network analysis identified six hub genes associated with rupture of intracranial aneurysms.PloS one · 2020Article
- KLHL3 single-nucleotide polymorphism is associated with essential hypertension in Chinese Han population.Medicine · 2019Article
- Mechanisms and controversies in mutant Cul3-mediated familial hyperkalemic hypertension.American journal of physiology. Renal physiology · 2018Review
- Article
- WNK Kinases in Development and Disease.Current topics in developmental biology · 2017Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic high blood pressure (hypertension) is the most common disease in the Unites States. While several classes of drugs exist to treat it, many patients (up to 10 million Americans) respond poorly to therapy, even when multiple classes are used. Recent evidence suggests that a significant portion of patients will always remain hypertensive despite maximum therapy with the drugs currently available. Therefore, there is a pressing need to develop novel antihypertensive agents. One limitation has been the identification of new targets, a limitation that has been overcome by recent insights into the mechanisms underlying monogenic forms of hypertension. The disease familial hyperkalemic hypertension is caused by mutations in with-no-lysine (WNK) kinases 1 and 4 and in cullin-3 and kelch-like 3, components of an E3 ubiquitin ligase complex that promotes WNK kinase degradation. The study of the mechanisms by which this pathway regulates blood pressure has identified several candidates for the development of new antihypertensive agents. This pathway is particularly attractive since its inhibition may not only reduce renal sodium reabsorption along multiple segments but may also reduce vascular tone. Here, we will describe the mechanisms by which this pathway regulate blood pressure and discuss the potential of targeting it to develop new antihypertensive drugs.
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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.