<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wu W</submitter><funding>Georgia State University</funding><pagination>1550</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8533440</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(10)</volume><pubmed_abstract>Heat shock protein 22 (Hsp22) is a small heat shock protein predominantly expressed in skeletal and cardiac muscle. Previous studies indicate that Hsp22 plays a vital role in protecting the heart against cardiac stress. However, the essential role of Hsp22 in the heart under physiological conditions remains largely unknown. In this study, we used an Hsp22 knockout (KO) mouse model to determine whether loss of Hsp22 impairs cardiac growth and function with increasing age under physiological conditions. Cardiac structural and functional alterations at baseline were measured using echocardiography and invasive catheterization in Hsp22 KO mice during aging transition compared to their age-matched wild-type (WT) littermates. Our results showed that Hsp22 deletion induced progressive cardiac dil</pubmed_abstract><journal>Antioxidants (Basel, Switzerland)</journal><pubmed_title>Hsp22 Deficiency Induces Age-Dependent Cardiac Dilation and Dysfunction by Impairing Autophagy, Metabolism, and Oxidative Response.</pubmed_title><pmcid>PMC8533440</pmcid><funding_grant_id>Faculty funds</funding_grant_id><pubmed_authors>Qiu H</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Xie M</pubmed_authors><pubmed_authors>Qin G</pubmed_authors><pubmed_authors>Wu W</pubmed_authors><pubmed_authors>Sun X</pubmed_authors><pubmed_authors>Lai L</pubmed_authors><pubmed_authors>Shi X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Hsp22 Deficiency Induces Age-Dependent Cardiac Dilation and Dysfunction by Impairing Autophagy, Metabolism, and Oxidative Response.</name><description>Heat shock protein 22 (Hsp22) is a small heat shock protein predominantly expressed in skeletal and cardiac muscle. Previous studies indicate that Hsp22 plays a vital role in protecting the heart against cardiac stress. However, the essential role of Hsp22 in the heart under physiological conditions remains largely unknown. In this study, we used an Hsp22 knockout (KO) mouse model to determine whether loss of Hsp22 impairs cardiac growth and function with increasing age under physiological conditions. Cardiac structural and functional alterations at baseline were measured using echocardiography and invasive catheterization in Hsp22 KO mice during aging transition compared to their age-matched wild-type (WT) littermates. Our results showed that Hsp22 deletion induced progressive cardiac dil</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Sep</publication><modification>2025-04-21T22:01:53.12Z</modification><creation>2025-04-21T22:01:53.12Z</creation></dates><accession>S-EPMC8533440</accession><cross_references><pubmed>34679684</pubmed><doi>10.3390/antiox10101550</doi></cross_references></HashMap>