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PIEZO1-mediated mechanosensation links aging to bladder dysfunction

Hamed, Y. M. F.; Joshi, V.; Wilhelm, K.; Romero, L. O.; Solomon, O. D.; Kwok, T. B.; Lopez Gonzalez, E. D.; Ridlon, M. M.; Pendyala, S.; Calhoun, C. M.; Martinez, A. E.; Asmussen, J. K.; Keil Stietz, K.; Vezina, C. M.; Vasquez, V.; Lichtarge, O.; Beyder, A.; Marshall, K. L.

2026-05-25 physiology
10.64898/2026.05.24.726025 bioRxiv
Show abstract

Aging is accompanied by profound changes in bladder function, leading to increased urinary frequency and incontinence that impair quality of life in humans and are recapitulated in mouse models. Bladder filling and emptying rely on precise mechanosensory feedback, yet how aging alters this sensory control remains unclear. PIEZO ion channels convert mechanical forces into cellular signals essential for bladder fullness sensation. Using inducible smooth-muscle specific Piezo1 deletion, we find that loss of Piezo1 attenuates aging-related bladder dysfunction. Dietary enrichment with margaric acid, a membrane-active fatty acid previously shown to inhibit PIEZO channels, reduced urinary dysfunction in aged mice. In humans, genotype-phenotype analyses reveal an association between a PIEZO1 gain-of-function variant and early-onset neuromuscular bladder dysfunction. Together, these findings define a smooth-muscle, PIEZO1-mediated mechanosensory basis for aging-related bladder dysfunction and introduce a non-invasive strategy for targeting PIEZO channels in vivo.

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"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.