<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(19)</volume><submitter>Huang Z</submitter><pubmed_abstract>Background Regulator of G protein signaling 6 ( RGS 6) is an important member of the RGS family and produces pleiotropic regulatory effects on cardiac pathophysiology. However, the role of RGS 6 protein in cardiomyocytes during angiotensin II - and pressure overload-induced cardiac hypertrophy remain unknown. Methods and Results Here, we used a genetic approach to study the regulatory role of RGS 6 in cardiomyocytes during pathological cardiac hypertrophy. RGS 6 expression was significantly increased in failing human hearts and in hypertrophic murine hearts. The extent of aortic banding-induced cardiac hypertrophy, dysfunction, and fibrosis in cardiac-specific RGS 6 knockout mice was alleviated, whereas the hearts of transgenic mice with cardiac-specific RGS 6 overexpression exhibited exac</pubmed_abstract><journal>Journal of the American Heart Association</journal><pagination>e009179</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6404897</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Regulator of G Protein Signaling 6 Facilities Cardiac Hypertrophy by Activating Apoptosis Signal-Regulating Kinase 1-P38/c-JUN N-Terminal Kinase 1/2 Signaling.</pubmed_title><pmcid>PMC6404897</pmcid><pubmed_authors>Xu N</pubmed_authors><pubmed_authors>Huang Z</pubmed_authors><pubmed_authors>Jiang W</pubmed_authors><pubmed_authors>Lu Y</pubmed_authors><pubmed_authors>Shu J</pubmed_authors><pubmed_authors>Cai J</pubmed_authors><pubmed_authors>Jiang M</pubmed_authors><pubmed_authors>Yuan H</pubmed_authors><pubmed_authors>Dai H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulator of G Protein Signaling 6 Facilities Cardiac Hypertrophy by Activating Apoptosis Signal-Regulating Kinase 1-P38/c-JUN N-Terminal Kinase 1/2 Signaling.</name><description>Background Regulator of G protein signaling 6 ( RGS 6) is an important member of the RGS family and produces pleiotropic regulatory effects on cardiac pathophysiology. However, the role of RGS 6 protein in cardiomyocytes during angiotensin II - and pressure overload-induced cardiac hypertrophy remain unknown. Methods and Results Here, we used a genetic approach to study the regulatory role of RGS 6 in cardiomyocytes during pathological cardiac hypertrophy. RGS 6 expression was significantly increased in failing human hearts and in hypertrophic murine hearts. The extent of aortic banding-induced cardiac hypertrophy, dysfunction, and fibrosis in cardiac-specific RGS 6 knockout mice was alleviated, whereas the hearts of transgenic mice with cardiac-specific RGS 6 overexpression exhibited exac</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Oct</publication><modification>2025-04-19T14:36:10.418Z</modification><creation>2019-08-04T07:22:51Z</creation></dates><accession>S-EPMC6404897</accession><cross_references><pubmed>30371330</pubmed><doi>10.1161/JAHA.118.009179</doi></cross_references></HashMap>