ArticleNature communications2026
Pyrimidinergic calcium signaling links tubular metabolism to fibrosis in kidney disease.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Dual action of baicalin against renal fibrosis in hyperuricemic nephropathy: targeting PANX1-P2Y6 signaling and gut microbiota dysbiosis.Journal of molecular histology · 2026Article
- Inhibition of (interstitial) P2YPflugers Archiv : European journal of physiology · 2026Article
- Inhibition of (interstitial) P2YResearch square · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) is a major global health problem, with substantial associated morbidity and mortality. Fibrosis is the final common pathway of organ damage in CKD, so understanding how this arises during kidney injury is critical for building a holistic picture of the pathogenesis. Here, using gene expression data, intravital microscopy in mice and realistic cell models, we uncover evidence of a signaling pathway linking tubular pyrimidine metabolism and injury-evoked extracellular uridine diphosphate (UDP) release to activation of the P2Y6 receptor (P2Y6R) in surrounding fibroblasts. We show that P2Y6R activation triggers intracellular calcium rises, which stimulate fibroblast proliferation, migration, and conversion towards a myofibroblast phenotype. Conversely, genetic knockout or pharmacological blockade of the P2Y6R reduces fibrosis in mice with CKD. Thus, we reveal that pyrimidinergic calcium signaling couples fibroblast responses to changes in tubular metabolism in disease states, and represents a potential new target for therapeutic intervention.
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