{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tang H"],"funding":["Health Commission of Sichuan Province Medical Science and Technology Program","National Natural Science Foundation of China","the First Affiliated Hospital of Chongqing Medical University, Doctoral Program of The First Affiliated Hospital of Chongqing Medical University","Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission","Natural Science Foundation of Sichuan Province"],"pagination":["13"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12798097"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["<h4>Background</h4>Ischemic stroke is a leading cause of morbidity and mortality worldwide, yet available therapeutic strategies remain limited. La ribonucleoprotein domain family member 7 (LARP7), a critical regulator of RNA stability and transcriptional control, participates in cellular stress responses and inflammatory modulation. Emerging evidence suggests LARP7's involvement in neuroinflammation and neuronal survival, yet its role in ischemic stroke pathogenesis is still poorly understood.<h4>Methods</h4>We systematically investigated LARP7 expression in patients with acute ischemic stroke (AIS), mice subjected to middle cerebral artery occlusion/reperfusion (MCAO/R), and neurons exposed to oxygen-glucose deprivation/reoxygenation (OGD/R). To elucidate the role of LARP7 in ischemic st"],"journal":["Journal of neuroinflammation"],"pubmed_title":["LARP7 protects against ischemic brain injury by modulating NLRP3 deacetylation to suppress neuronal pyroptosis."],"pmcid":["PMC12798097"],"funding_grant_id":["82171456","CYYY-BSYJSCXXM-202327","2025ZNSFSC0589","cstc2021jcyj-msxmX0263","24WSXT075","24QNMP024"],"pubmed_authors":["Li J","Li C","Huang J","Ren Y","Qin T","Zi W","Zhao Y","Tang H","Wang L","Wen J","He Y","Yang Q","Wu Y"],"additional_accession":[]},"is_claimable":false,"name":"LARP7 protects against ischemic brain injury by modulating NLRP3 deacetylation to suppress neuronal pyroptosis.","description":"<h4>Background</h4>Ischemic stroke is a leading cause of morbidity and mortality worldwide, yet available therapeutic strategies remain limited. La ribonucleoprotein domain family member 7 (LARP7), a critical regulator of RNA stability and transcriptional control, participates in cellular stress responses and inflammatory modulation. Emerging evidence suggests LARP7's involvement in neuroinflammation and neuronal survival, yet its role in ischemic stroke pathogenesis is still poorly understood.<h4>Methods</h4>We systematically investigated LARP7 expression in patients with acute ischemic stroke (AIS), mice subjected to middle cerebral artery occlusion/reperfusion (MCAO/R), and neurons exposed to oxygen-glucose deprivation/reoxygenation (OGD/R). To elucidate the role of LARP7 in ischemic st","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-06T15:21:04.981Z","creation":"2026-06-01T03:11:05.492Z"},"accession":"S-EPMC12798097","cross_references":{"pubmed":["41351020"],"doi":["10.1186/s12974-025-03649-3"]}}