ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026
[PGAM5 deficiency attenuates atherosclerosis, enhances oxidized LDL uptake by liver sinusoidal endothelial cells and reshapes circulating lipidome in mice].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 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
objectivesTo investigate the effects of mitochondrial phosphoglycerate mutase 5 (PGAM5) deficiency on endocytic function of liver sinusoidal endothelial cells (LSECs) and circulating lipid remodeling and their association with atherosclerosis (AS).
methodsAS was induced by tail vein injection of AAV-PCSK9 combined with Western diet (WD) feeding. Mice were divided into 5 groups: NC (negative control, normal chow feeding), ND (normal chow feeding after AAV-PCSK9 injection), WD (WD feeding after AAV-PCSK9 injection), ATOR (WD feeding plus atorvastatin calcium gavage after AAV-PCSK9 injection), and PGAM5 KO (PGAM5
resultsHepatic PGAM5 expression increased in AS. Compared with NC, WD mice showed increased aortic plaque burden, hepatic steatosis, and LDL-C abnormalities. Compared with WD, PGAM5 KO mice showed reduced aortic lipid deposition, enhanced plaque stability, decreased plasma low-density lipoprotein cholesterol (LDL-C) levels, and improved hepatic steatosis. Liver proteomics revealed differential protein enrichment in fatty acid metabolism and endocytosis pathways. Single-cell RNA-seq showed altered relative LSEC proportions following PGAM5 deficiency. Plasma metabolomics showed decreased L-palmitoylcarnitine (L-PC) and arachidonic acid (AA) levels in PGAM5
conclusionsPGAM5 deficiency is associated with enhanced endocytic function of LSECs and circulating lipid remodeling, which may contribute to ameliorated AS.
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