{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(19)"],"submitter":["Huang Z"],"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"],"journal":["Journal of the American Heart Association"],"pagination":["e009179"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6404897"],"repository":["biostudies-literature"],"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."],"pmcid":["PMC6404897"],"pubmed_authors":["Xu N","Huang Z","Jiang W","Lu Y","Shu J","Cai J","Jiang M","Yuan H","Dai H"],"additional_accession":[]},"is_claimable":false,"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.","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","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Oct","modification":"2025-04-19T14:36:10.418Z","creation":"2019-08-04T07:22:51Z"},"accession":"S-EPMC6404897","cross_references":{"pubmed":["30371330"],"doi":["10.1161/JAHA.118.009179"]}}