<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zigmond ZM</submitter><funding>BLRD VA</funding><funding>NIDDK NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>American Heart Association Inc</funding><funding>NIH</funding><pagination>133-140</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8096668</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>324</volume><pubmed_abstract>&lt;h4>Background and aims&lt;/h4>Increased receptor tyrosine kinase (RTK) activity has been historically linked to atherosclerosis. Paradoxically, we recently found that global deficiency in c-Kit function increased atherosclerosis in hyperlipidemic mice. This study aimed to investigate if such unusual atheroprotective phenotype depends upon c-Kit's function in smooth muscle cells (SMC).&lt;h4>Methods&lt;/h4>We studied atherosclerosis in a SMC-specific conditional knockout mice (Kit&lt;sup>SMC&lt;/sup>) and control littermate. Tamoxifen (TAM) and vehicle treated mice were fed high fat diet for 16 weeks before atherosclerosis assessment in the whole aorta using oil red staining. Smooth muscle cells were traced within the aortic sinus of conditional c-Kit tracing mice (Kit&lt;sup>SMC&lt;/sup> eYFP) and their contr</pubmed_abstract><journal>Atherosclerosis</journal><pubmed_title>c-Kit expression in smooth muscle cells reduces atherosclerosis burden in hyperlipidemic mice.</pubmed_title><pmcid>PMC8096668</pmcid><funding_grant_id>R01 HL125672</funding_grant_id><funding_grant_id>R01 DK121227</funding_grant_id><funding_grant_id>K01 HL145359</funding_grant_id><funding_grant_id>K08 HL151747</funding_grant_id><funding_grant_id>I01 BX004658</funding_grant_id><pubmed_authors>Song L</pubmed_authors><pubmed_authors>Vazquez-Padron RI</pubmed_authors><pubmed_authors>Martinez L</pubmed_authors><pubmed_authors>Zigmond ZM</pubmed_authors><pubmed_authors>Velazquez OC</pubmed_authors><pubmed_authors>Lassance-Soares RM</pubmed_authors></additional><is_claimable>false</is_claimable><name>c-Kit expression in smooth muscle cells reduces atherosclerosis burden in hyperlipidemic mice.</name><description>&lt;h4>Background and aims&lt;/h4>Increased receptor tyrosine kinase (RTK) activity has been historically linked to atherosclerosis. Paradoxically, we recently found that global deficiency in c-Kit function increased atherosclerosis in hyperlipidemic mice. This study aimed to investigate if such unusual atheroprotective phenotype depends upon c-Kit's function in smooth muscle cells (SMC).&lt;h4>Methods&lt;/h4>We studied atherosclerosis in a SMC-specific conditional knockout mice (Kit&lt;sup>SMC&lt;/sup>) and control littermate. Tamoxifen (TAM) and vehicle treated mice were fed high fat diet for 16 weeks before atherosclerosis assessment in the whole aorta using oil red staining. Smooth muscle cells were traced within the aortic sinus of conditional c-Kit tracing mice (Kit&lt;sup>SMC&lt;/sup> eYFP) and their contr</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 May</publication><modification>2025-04-04T10:17:11.491Z</modification><creation>2025-04-04T10:17:11.491Z</creation></dates><accession>S-EPMC8096668</accession><cross_references><pubmed>33781566</pubmed><doi>10.1016/j.atherosclerosis.2021.03.004</doi></cross_references></HashMap>