<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Snarski P</submitter><funding>NHLBI NIH HHS</funding><pagination>113-126</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8792341</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(2)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>IGF-1 (insulin-like growth factor 1) exerts pleiotropic effects including promotion of cellular growth, differentiation, survival, and anabolism. We have shown that systemic IGF-1 administration reduced atherosclerosis in Apoe&lt;sup>-/&lt;/sup>&lt;sup>-&lt;/sup> (apolipoprotein E deficient) mice, and this effect was associated with a reduction in lesional macrophages and a decreased number of foam cells in the plaque. Almost all cell types secrete IGF-1, but the effect of macrophage-derived IGF-1 on the pathogenesis of atherosclerosis is poorly understood. We hypothesized that macrophage-derived IGF-1 will reduce atherosclerosis. Approach and Results: We created macrophage-specific IGF-1 overexpressing mice on an Apoe&lt;sup>-&lt;/sup>&lt;sup>/&lt;/sup>&lt;sup>-&lt;/sup> background. Macrophage-specif</pubmed_abstract><journal>Arteriosclerosis, thrombosis, and vascular biology</journal><pubmed_title>Macrophage-Specific IGF-1 Overexpression Reduces CXCL12 Chemokine Levels and Suppresses Atherosclerotic Burden in Apoe-Deficient Mice.</pubmed_title><pmcid>PMC8792341</pmcid><funding_grant_id>R01 HL142796</funding_grant_id><funding_grant_id>R01 HL070241</funding_grant_id><pubmed_authors>Sukhanov S</pubmed_authors><pubmed_authors>Danchuk S</pubmed_authors><pubmed_authors>Higashi Y</pubmed_authors><pubmed_authors>Chandrasekar B</pubmed_authors><pubmed_authors>Yoshida T</pubmed_authors><pubmed_authors>Snarski P</pubmed_authors><pubmed_authors>Rivera-Lopez V</pubmed_authors><pubmed_authors>Tian D</pubmed_authors><pubmed_authors>Delafontaine P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Macrophage-Specific IGF-1 Overexpression Reduces CXCL12 Chemokine Levels and Suppresses Atherosclerotic Burden in Apoe-Deficient Mice.</name><description>&lt;h4>Objective&lt;/h4>IGF-1 (insulin-like growth factor 1) exerts pleiotropic effects including promotion of cellular growth, differentiation, survival, and anabolism. We have shown that systemic IGF-1 administration reduced atherosclerosis in Apoe&lt;sup>-/&lt;/sup>&lt;sup>-&lt;/sup> (apolipoprotein E deficient) mice, and this effect was associated with a reduction in lesional macrophages and a decreased number of foam cells in the plaque. Almost all cell types secrete IGF-1, but the effect of macrophage-derived IGF-1 on the pathogenesis of atherosclerosis is poorly understood. We hypothesized that macrophage-derived IGF-1 will reduce atherosclerosis. Approach and Results: We created macrophage-specific IGF-1 overexpressing mice on an Apoe&lt;sup>-&lt;/sup>&lt;sup>/&lt;/sup>&lt;sup>-&lt;/sup> background. Macrophage-specif</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-05T09:04:52.865Z</modification><creation>2025-04-05T09:04:52.865Z</creation></dates><accession>S-EPMC8792341</accession><cross_references><pubmed>34852642</pubmed><doi>10.1161/ATVBAHA.121.316090</doi><doi>10.1161/atvbaha.121.316090</doi></cross_references></HashMap>