{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Barrick CJ"],"funding":["Burroughs Wellcome Fund Career Award in Biomedical Sciences","American Heart Association Established Investigator Award","NHLBI NIH HHS"],"pagination":["165-74"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3256744"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["52(1)"],"pubmed_abstract":["Sex differences exist in the hypertrophic response, cardiac remodeling, and transition to heart failure of hypertensive patients, and while some of these differences are likely influenced by estrogen, the genetic pathways downstream of estrogen that impact on cardioprotection have yet to be fully elucidated. We have previously shown that the cardioprotective effects of adrenomedullin (AM), an emerging clinical biomarker for cardiovascular disease severity, vary with sex in mouse models. AM signaling during cardiovascular stress is strongly modulated by receptor activity-modifying protein 3 (RAMP3) via its interaction with the G protein-coupled receptor calcitonin receptor-like receptor (CLR). Like AM, RAMP3 expression is potently regulated by estrogen, and so we sought to determine the con"],"journal":["Journal of molecular and cellular cardiology"],"pubmed_title":["Loss of receptor activity-modifying protein 3 exacerbates cardiac hypertrophy and transition to heart failure in a sex-dependent manner."],"pmcid":["PMC3256744"],"funding_grant_id":["R01 HL091973-03","HL091973","R01 HL091973","F30 HL104778"],"pubmed_authors":["Lenhart PM","Dackor RT","Nagle E","Caron KM","Barrick CJ"],"additional_accession":[]},"is_claimable":false,"name":"Loss of receptor activity-modifying protein 3 exacerbates cardiac hypertrophy and transition to heart failure in a sex-dependent manner.","description":"Sex differences exist in the hypertrophic response, cardiac remodeling, and transition to heart failure of hypertensive patients, and while some of these differences are likely influenced by estrogen, the genetic pathways downstream of estrogen that impact on cardioprotection have yet to be fully elucidated. We have previously shown that the cardioprotective effects of adrenomedullin (AM), an emerging clinical biomarker for cardiovascular disease severity, vary with sex in mouse models. AM signaling during cardiovascular stress is strongly modulated by receptor activity-modifying protein 3 (RAMP3) via its interaction with the G protein-coupled receptor calcitonin receptor-like receptor (CLR). Like AM, RAMP3 expression is potently regulated by estrogen, and so we sought to determine the con","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Jan","modification":"2025-04-04T21:13:26.292Z","creation":"2019-03-26T23:05:09Z"},"accession":"S-EPMC3256744","cross_references":{"pubmed":["22100352"],"doi":["10.1016/j.yjmcc.2011.10.021"]}}