RSK3: A regulator of pathological cardiac remodeling

被引:16
|
作者
Martinez, Eliana C. [1 ]
Passariello, Catherine L. [1 ]
Li, Jinliang [1 ]
Matheson, Christopher J. [2 ]
Dodge-Kafka, Kimberly [3 ]
Reigan, Philip [2 ]
Kapiloff, Michael S. [1 ]
机构
[1] Univ Miami, Miller Sch Med, Cardiac Signal Transduct & Cellular Biol Lab, Interdisciplinary Stem Cell Inst,Div Cardiol,Dept, Miami, FL 33101 USA
[2] Univ Colorado, Skaggs Sch Pharm & Pharmaceut Sci, Dept Pharmaceut Sci, Aurora, CO USA
[3] Univ Connecticut, Ctr Hlth, Calhoun Ctr Cardiol, Farmington, CT USA
关键词
Keywords ribosomal S6 kinase; heart; hypertrophy; remodeling; signal transduction; scaffold; mAKAP; RIBOSOMAL S6 KINASE; ACTIVATED PROTEIN-KINASE; ATTENUATES HYPERTROPHIC RESPONSE; RYANODINE RECEPTOR; TARGETED DELETION; SIGNALING COMPLEX; OXIDATIVE STRESS; HEART-FAILURE; INHIBITOR; MAKAP;
D O I
10.1002/iub.1383
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The family of p90 ribosomal S6 kinases (RSKs) are pleiotropic effectors for extracellular signal-regulated kinase signaling pathways. Recently, RSK3 was shown to be important for pathological remodeling of the heart. Although cardiac myocyte hypertrophy can be compensatory for increased wall stress, in chronic heart diseases, this nonmitotic cell growth is usually associated with interstitial fibrosis, increased cell death, and decreased cardiac function. Although RSK3 is less abundant in the cardiac myocyte than other RSK family members, RSK3 appears to serve a unique role in cardiac myocyte stress responses. A potential mechanism conferring the unique function of RSK3 in the heart is anchoring by the scaffold protein muscle A-kinase anchoring protein (mAKAP). Recent findings suggest that RSK3 should be considered as a therapeutic target for the prevention of heart failure, a clinical syndrome of major public health significance. (c) 2015 IUBMB Life, 2015 67(5):331-337, 2015
引用
收藏
页码:331 / 337
页数:7
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