ArticleRenal failure2026
Virtual screening and cellular validation of dolutegravir as a BRD9 inhibitor for attenuating pyroptosis in peritoneal mesothelial cells.
Article in Renal failure, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPeritoneal dialysis is an essential therapy for end-stage renal disease; however, long-term exposure to high-glucose dialysis solutions induces pyroptosis of peritoneal mesothelial cells, promoting peritoneal fibrosis and ultimately leading to technique failure. The involvement of the epigenetic regulator bromodomain-containing protein 9 (BRD9) in this process remains unclear.
methodsStructure-based virtual screening of 3,447 FDA-approved drugs from the ZINC database identified dolutegravir as a candidate BRD9 inhibitor. Direct binding and inhibitory activity were validated using cellular thermal shift assays, IC
resultsDolutegravir directly bound to and inhibited BRD9. Under high-glucose stimulation, dolutegravir markedly suppressed NLRP3 inflammasome activation, reduced caspase-1 and gasdermin D cleavage, and decreased interleukin (IL)-1β and IL-18 maturation and release. Mechanistically, BRD9 inhibition accelerated nod-like receptor protein 3 (NLRP3) mRNA degradation and attenuated NLRP3-mediated secretion of the pro-fibrotic factor transforming growth factor-beta 1, leading to downregulation of fibrosis-related markers smooth muscle alpha-actin 2 and collagen type I alpha 1.
conclusionThis study identifies dolutegravir as a novel BRD9 inhibitor and demonstrates that BRD9 is a key regulator of high glucose-induced pyroptosis and pro-fibrotic signaling in mesothelial cells
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