ArticleThe Journal of clinical investigation2025
KS-WNK1 augments the effects of dietary potassium intake on renal sodium chloride reabsorption.
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 1 paper.
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
1 citing paper in PubMed.
- The exquisite link between potassium homeostasis regulation and cardiovascular health: exploration and analysis.Frontiers in physiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinically, potassium supplementation has been shown to lower blood pressure and reduce the risk of stroke through modulation of potassium excretion and sodium reabsorption. Hypokalemia activates the renal sodium chloride cotransporter (NCC) along the distal convoluted tubule (DCT), at least in part, through with-no-lysine 4 (WNK4) kinase and STE20/SPS1-related proline-alanine-rich protein kinase (SPAK) signaling. The DCT also expresses a kinase-deficient, kidney-specific form of WNK1 (KS-WNK1), but its role in NCC activation is unclear. In this issue of the JCI, Boyd-Shiwarski and colleagues found that KS-WNK1 enhanced the effects of potassium on NCC activation in vivo. Specifically, they showed that mice lacking KS-WNK1 did not respond as robustly to dietary challenge. Additionally, in vivo expression of a mutated KS-WNK1 disrupted WNK body, or biomolecular condensate, formation and renal function. These findings, along with those of previous studies, indicate that KS-WNK1 may regulate potassium homeostasis by increasing the kidney's sensitivity to salt-dependent stress.
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.