ArticlePflugers Archiv : European journal of physiology2025
Hyperosmolality activates polycystin-2 and TRPM4 in renal primary cilium.
Article in Pflugers Archiv : European journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Primary cilia: master conductors of cellular communication in development and disease.Nature reviews. Nephrology · 2026Review
- Abnormal purinergic signaling contributes to development of renal cysts in autosomal dominant polycystic kidney disease.Purinergic signalling · 2026Article
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Authors and funding
1 author.
Funding
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Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is a debilitating disease characterized by renal cysts. It arises from mutations in proteins expressed in part in the primary cilia of renal epithelial cells. One of these, polycystin-2 (PC2), is an ion-conducting channel. To date, ion channels in the cilium have only been characterized in standard normosmolar external solutions, but the osmolality of the renal filtrate bathing the cilia varies widely. Here I report that urine, which better represents the filtrate, activates a large cation-conducting current in the cilia. With defined external solutions, hyperosmolality through addition of urea, NaCl, or D-mannitol activates a similar current. Most but not all of this current is conducted through TRPM4 channels. It is greatly reduced by internal MgATP or 9-phenanthrol, which inhibit TRPM4, or by shRNA knockdown of TRPM4. However, part of the current activated by urea conducts Ca
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