GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE345nnn/GSE345117/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE345117GEOGSEfalseSulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cellsAcute lung injury (ALI) is a critical disease with high mortality, yet its mechanisms remain incompletely elucidated. In this study we investigated sulfonylurea receptor 1 (SUR1), the regulatory subunit of ATP-sensitive potassium (KATP) channels, in the progression of ALI. We observed elevated SUR1 protein levels in the bronchial alveolar lavage fluid (BALF) of patients with sepsis-associated ALI, as well as in BALF and lung tissues of ALI mouse models. Genetic deletion of SUR1, but not Kir6.2 (the pore-forming subunit of KATP channels), significantly alleviated ALI induced by cecal ligation and puncture (CLP) or by lipopolysaccharide (LPS) intratracheal instillation. Mechanistically, SUR1 interacted with poly (ADP-ribose) polymerase 1 (PARP1), impairing DNA damage repair and promoting apoptosis and NF-κB (nuclear factor kappa B) activation in bronchial epithelial cells. Notably, glibenclamide, a clinically approved SUR1 inhibitor, significantly alleviated ALI, at least in part, by disrupting the SUR1–PARP1 interaction. Our findings identify SUR1 as a new therapeutic target and highlighting the potential repurposing of glibenclamide as a therapeutic drug in ALI.2026/08/26GSE345117GSM9996776GSM9996777GSM9996778GSM9996779GSM9996774GSM999677529480345117Homo sapiens