ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
The GPX3-VCAM1 Axis Gates Pro-Fibrotic Tubule Cell Fate in Hyperuricemic Nephropathy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Hyperuricemia is a major driver of chronic kidney disease, yet the underlying intrarenal mechanisms remain unclear. Here, we establish a genetically defined, multi-hit mouse model that recapitulates the sustained hyperuricemia, metabolic dysregulation, and progressive fibrosis of human disease. Using this model, we demonstrate that soluble uric acid activates the renal NLRP3 inflammasome and that its inhibition attenuates kidney injury. Single-nucleus RNA sequencing revealed a distinct pro-inflammatory and pro-fibrotic proximal tubule cell population (Profib PT) marked by high VCAM1 expression, which is conserved in human kidney disease. Direct VCAM1 neutralization with antibodies attenuated renal fibrosis, validating its functional role. Mechanistically, we identify glutathione peroxidase 3 (GPX3) as a master regulator restraining precursor cell differentiation into Profib PT cells. GPX3 expression is suppressed in hyperuricemia, licensing this pathogenic transition; conversely, dietary selenium supplementation restored GPX3 activity, blocked Profib PT differentiation and VCAM1-dependent macrophage adhesion, and ameliorated renal fibrosis. Our findings define the GPX3-VCAM1 axis as a central regulatory node in hyperuricemic nephropathy and identify nutritional selenium repletion as a novel therapeutic strategy to intercept fibrosis.
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.