title: RASSF1A: a potential novel therapeutic target against cardiac hypertrophy.
abstract: Cardiac hypertrophy is a key risk factor for chronic heart failure. Current treatments predominantly focus on both reducing the peripheral vascular resistance and activating nerve-humoral system. However, these efforts can't reverse cardiac hypertrophy fundamentally. Ras association domain family 1 isoform A (RASSF1A) is a regulatory tumor suppressor whose inactivation by inappropriate promoter methylation has been implicated in the development of many human cancers. Recently, there have been a number of studies investigating the roles of RASSF1A in the pathophysiology of cardiac hypertrophy. In this review, we focus on the present progresses of cardiac RASSF1A under physiological and pathological conditions, trying to systematically elucidate how the RASSF1A-mediated signal pathways contribute to the maintenance of normal cardiac myocyte structure and function and lead to the regression of pathological cardiac hypertrophy. These pathways exert multiple functions such as regulating cardiac contractility, physiologically increasing stability of microtubule, preventing cardiac dysfunction, attenuating interstitial fibrosis and mediating cell apoptosis. These specific roles are highly relevant with cardiac hemodynamics and therapeutic strategies, indicating RASSF1A may have the potential to reverse pathological cardiac hypertrophy thus prevent heart failure fundamentally.
authors.affiliation: Company Five of Cadet Brigade, Third Military Medical University, Chongqing 400038, China.
authors.forename: Chenyang
authors.initials: C
authors.lastname: Duan
authors.forename: Mengying
authors.initials: M
authors.lastname: Liu
authors.forename: Jiqiang
authors.initials: J
authors.lastname: Zhang
authors.forename: Ruiyan
authors.initials: R
authors.lastname: Ma
mesh_terms: D006332:Cardiomegaly / Q000188:drug therapy* / Q000503:physiopathology*; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D006801:Humans; D008955:Models, Cardiovascular; D058990:Molecular Targeted Therapy / Q000379:methods*; D015398:Signal Transduction / Q000187:drug effects*; D025521:Tumor Suppressor Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism*
chemical_list: D002316:Cardiotonic Agents; C411762:RASSF1 protein, human; D025521:Tumor Suppressor Proteins
keywords: Cardiac hypertrophy; Heart failure; Ras association domain family 1 isoform A; Signaling pathway; Therapeutic strategy