ArticleAmerican journal of physiology. Renal physiology2019
Regulation of the renal NaCl cotransporter by the WNK/SPAK pathway: lessons learned from genetically altered animals.
Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Monogenic Kidney Disorders as Hidden Drivers of Electrolyte Imbalance and Hypertension.Electrolyte & blood pressure : E & BP · 2026Review
- Structural bases for NaNature communications · 2024Article
- Thirty years of the NaCl cotransporter: from cloning to physiology and structure.American journal of physiology. Renal physiology · 2023Review
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Structural basis for inhibition of the Cation-chloride cotransporter NKCC1 by the diuretic drug bumetanide.Nature communications · 2022Article
- A narrative review of Hyporeninemic hypertension-an indicator for monogenic forms of hypertension.Pediatric medicine (Hong Kong, China) · 2022Article
- Molecular mechanisms for the modulation of blood pressure and potassium homeostasis by the distal convoluted tubule.EMBO molecular medicine · 2022Review
- Role of KLHL3 and dietary KAmerican journal of physiology. Renal physiology · 2021Article
- A rare case of hyporeninemic hypertension: Answers.Pediatric nephrology (Berlin, Germany) · 2021Article
- Review
- Familial Hyperkalemic Hypertension Genotype With a Negative Phenotype: A CUL3 Mosaicism.American journal of hypertension · 2020Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The renal thiazide-sensitive NaCl cotransporter (NCC) is the major salt transport pathway in the distal convoluted tubule of the mammalian nephron. NCC activity is critical for modulation of arterial blood pressure and serum potassium levels. Reduced activity of NCC in genetic diseases results in arterial hypotension and hypokalemia, while increased activity results in genetic diseases featuring hypertension and hyperkalemia. Several hormones and physiological conditions modulate NCC activity through a final intracellular complex pathway involving kinases and ubiquitin ligases. A substantial amount of work has been conducted to understand this pathway in the last 15 yr, but advances over the last 3 yr have helped to begin to understand how these regulatory proteins interact with each other and modulate the activity of this important cotransporter. In this review, we present the current model of NCC regulation by the Cullin 3 protein/Kelch-like 3 protein/with no lysine kinase/STE20-serine-proline alanine-rich kinase (CUL3/KELCH3-WNK-SPAK) pathway. We present a review of all genetically altered mice that have been used to translate most of the proposals made from in vitro experiments into in vivo observations that have helped to elucidate the model at the physiological level. Many questions have been resolved, but some others will require further models to be constructed. In addition, unexpected observations in mice have raised new questions and identified regulatory pathways that were previously unknown.
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