ArticleThe Journal of clinical investigation2025
Kidney-specific WNK1 amplifies kidney tubule responsiveness to potassium via WNK body condensates.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- The kidney distal tubule potassium switch, modern diet and hypertension.Nature reviews. Nephrology · 2026Review
- Monogenic Kidney Disorders as Hidden Drivers of Electrolyte Imbalance and Hypertension.Electrolyte & blood pressure : E & BP · 2026Review
- Potassium and the kidney.Nature reviews. Nephrology · 2026Review
- The Story of Aldosterone Escape.Journal of the American Society of Nephrology : JASN · 2026Review
- Targeting WNK1 suppresses acute myeloid leukemia progression and enhances sensitivity to venetoclax.Frontiers in oncology · 2026Article
- KS-WNK1 augments the effects of dietary potassium intake on renal sodium chloride reabsorption.The Journal of clinical investigation · 2025Article
- The evolving concepts of KS-WNK1 effect on NCC activity.American journal of physiology. Renal physiology · 2025Review
- Molecular Crowding: Physiologic Sensing and Control.Annual review of physiology · 2024Review
- Review
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
To maintain potassium homeostasis, the kidney's distal convoluted tubule (DCT) evolved to convert small changes in blood [K+] into robust effects on salt reabsorption. This process requires NaCl cotransporter (NCC) activation by the with-no-lysine (WNK) kinases. During hypokalemia, the kidney-specific WNK1 isoform (KS-WNK1) scaffolds the DCT-expressed WNK signaling pathway within biomolecular condensates of unknown function termed WNK bodies. Here, we show that KS-WNK1 amplified kidney tubule reactivity to blood [K+], in part via WNK bodies. In genetically modified mice, targeted condensate disruption trapped the WNK pathway, causing renal salt wasting that was more pronounced in females. In humans, WNK bodies accumulated as plasma potassium fell below 4.0 mmol/L, suggesting that the human DCT experiences the stress of potassium deficiency, even when [K+] is in the low-to-normal range. These data identify WNK bodies as kinase signal amplifiers that mediate tubular [K+] responsiveness, nephron sexual dimorphism, and BP salt sensitivity. Our results illustrate how biomolecular condensate specialization can optimize a mammalian physiologic stress response that impacts human health.
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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.