<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zahr T</submitter><funding>NIDDK NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>30-44</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9917767</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Atherosclerosis is a medical urgency manifesting at the onset of hypercholesterolemia and is associated with aging. Activation of PPARγ (peroxisome proliferator-activated receptor γ) counteracts metabolic dysfunction influenced by aging, and its deacetylation displays an atheroprotective property. Despite the marked increase of PPARγ acetylation during aging, it is unknown whether PPARγ acetylation is a pathogenic contributor to aging-associated atherosclerosis.&lt;h4>Methods&lt;/h4>Mice with constitutive deacetylation-mimetic PPARγ mutations on lysine residues K268 and K293 (2KR) in an LDL (low-density lipoprotein)-receptor knockout (&lt;i>Ldlr&lt;/i>&lt;sup>-/-&lt;/sup>) background (&lt;i>2KR:Ldlr&lt;/i>&lt;sup>-/-&lt;/sup>) were aged for 18 months on a standard laboratory diet to examine the cardi</pubmed_abstract><journal>Arteriosclerosis, thrombosis, and vascular biology</journal><pubmed_title>PPARγ (Peroxisome Proliferator-Activated Receptor γ) Deacetylation Suppresses Aging-Associated Atherosclerosis and Hypercholesterolemia.</pubmed_title><pmcid>PMC9917767</pmcid><funding_grant_id>P01 HL087123</funding_grant_id><funding_grant_id>R01 DK131169</funding_grant_id><funding_grant_id>R35 GM147269</funding_grant_id><funding_grant_id>R01 DK112943</funding_grant_id><funding_grant_id>R01 DK128848</funding_grant_id><funding_grant_id>R00 DK115778</funding_grant_id><pubmed_authors>Cai B</pubmed_authors><pubmed_authors>Sun L</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Chan M</pubmed_authors><pubmed_authors>Zhou Q</pubmed_authors><pubmed_authors>He Y</pubmed_authors><pubmed_authors>Accili D</pubmed_authors><pubmed_authors>Zahr T</pubmed_authors><pubmed_authors>Aaron N</pubmed_authors><pubmed_authors>Qiang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>PPARγ (Peroxisome Proliferator-Activated Receptor γ) Deacetylation Suppresses Aging-Associated Atherosclerosis and Hypercholesterolemia.</name><description>&lt;h4>Background&lt;/h4>Atherosclerosis is a medical urgency manifesting at the onset of hypercholesterolemia and is associated with aging. Activation of PPARγ (peroxisome proliferator-activated receptor γ) counteracts metabolic dysfunction influenced by aging, and its deacetylation displays an atheroprotective property. Despite the marked increase of PPARγ acetylation during aging, it is unknown whether PPARγ acetylation is a pathogenic contributor to aging-associated atherosclerosis.&lt;h4>Methods&lt;/h4>Mice with constitutive deacetylation-mimetic PPARγ mutations on lysine residues K268 and K293 (2KR) in an LDL (low-density lipoprotein)-receptor knockout (&lt;i>Ldlr&lt;/i>&lt;sup>-/-&lt;/sup>) background (&lt;i>2KR:Ldlr&lt;/i>&lt;sup>-/-&lt;/sup>) were aged for 18 months on a standard laboratory diet to examine the cardi</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-04T03:01:01.945Z</modification><creation>2025-04-04T03:01:01.945Z</creation></dates><accession>S-EPMC9917767</accession><cross_references><pubmed>36453279</pubmed><doi>10.1161/ATVBAHA.122.318061</doi><doi>10.1161/atvbaha.122.318061</doi></cross_references></HashMap>