{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yi H"],"funding":["Natural Science Foundation of Jilin Province"],"pagination":["e70048"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12484710"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(4)"],"pubmed_abstract":["Abdominal aortic aneurysm (AAA) is a life-threatening vascular disorder lacking effective pharmacological interventions. We identified CD5 molecule-like (CD5L) as a regulator of macrophage polarization in AAA via the phosphoinositide 3-kinase/protein kinase B/nuclear factor kappa B (PI3K/Akt/NF-κB) pathway. Transcriptomic analyses (GSE47472 and GSE57691) and angiotensin II (AngII)-infused apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice showed CD5L upregulation, inversely correlated with M1 macrophage infiltration. In vitro CD5L overexpression reduced, whereas knockdown increased M1 polarization and pro-inflammatory cytokines in RAW264.7 cells and human monocyte-derived macrophages. In vivo, CD5L knockdown aggravated aortic dilation, vascular disruption, and inflammatory mediator expre"],"journal":["Journal of cell communication and signaling"],"pubmed_title":["Targeting the PI3K/Akt/NF-κB axis: Cluster of differentiation 5-like-mediated immunometabolic regulation of macrophage polarization in abdominal aortic aneurysm."],"pmcid":["PMC12484710"],"funding_grant_id":["20230203582JC"],"pubmed_authors":["Wu Z","Yi H","Duan M","Li T","Liu N","Liu Q","Li L","Wan T"],"additional_accession":[]},"is_claimable":false,"name":"Targeting the PI3K/Akt/NF-κB axis: Cluster of differentiation 5-like-mediated immunometabolic regulation of macrophage polarization in abdominal aortic aneurysm.","description":"Abdominal aortic aneurysm (AAA) is a life-threatening vascular disorder lacking effective pharmacological interventions. We identified CD5 molecule-like (CD5L) as a regulator of macrophage polarization in AAA via the phosphoinositide 3-kinase/protein kinase B/nuclear factor kappa B (PI3K/Akt/NF-κB) pathway. Transcriptomic analyses (GSE47472 and GSE57691) and angiotensin II (AngII)-infused apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice showed CD5L upregulation, inversely correlated with M1 macrophage infiltration. In vitro CD5L overexpression reduced, whereas knockdown increased M1 polarization and pro-inflammatory cytokines in RAW264.7 cells and human monocyte-derived macrophages. In vivo, CD5L knockdown aggravated aortic dilation, vascular disruption, and inflammatory mediator expre","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-04T02:28:08.966Z","creation":"2026-05-04T03:13:28.132Z"},"accession":"S-EPMC12484710","cross_references":{"pubmed":["41040887"],"doi":["10.1002/ccs3.70048"]}}