Molecular Aspects of Exercise-induced Cardiac Remodeling

被引：28

作者：

Bernardo, Bianca C. ^{[1
]}

McMullen, Julie R. ^{[1
,2
,3
]}

机构：

[1] Baker IDI Heart & Diabet Inst, Cardiac Hypertrophy Lab, POB 6492, Melbourne, Vic 3004, Australia

[2] Monash Univ, Cent Clin Sch, Dept Med, 99 Commercial Rd, Melbourne, Vic 3004, Australia

[3] Monash Univ, Dept Physiol, Wellington Rd, Clayton, Vic 3800, Australia

来源：

CARDIOLOGY CLINICS | 2016年 / 34卷 / 04期

关键词：

Exercise; Cardiac remodeling; Molecular mechanisms; Cardiac myocyte; Cardiac hypertrophy; Drug targets; LEFT-VENTRICULAR HYPERTROPHY; PHOSPHOINOSITIDE 3-KINASE P110-ALPHA; CARDIOMYOCYTE DNA-SYNTHESIS; CROSS-COUNTRY SKIERS; ALL-CAUSE MORTALITY; AEROBIC EXERCISE; HEART-FAILURE; MYOCARDIAL-INFARCTION; PATHOLOGICAL HYPERTROPHY; CIRCULATING MICRORNAS;

D O I：

10.1016/j.ccl.2016.06.002

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Exercise-induced cardiac remodeling is typically an adaptive response associated with cardiac myocyte hypertrophy and renewal, increased cardiac myocyte contractility, sarcomeric remodeling, cell survival, metabolic and mitochondria! adaptations, electrical remodeling, and angiogenesis. Initiating stimuli/triggers of cardiac remodeling include increased hemodynamic load, increased sympathetic activity, and the release of hormones and growth factors. Prolonged and strenuous exercise may lead to maladaptive exercise-induced cardiac remodeling including cardiac dysfunction and arrhythmia. In addition, this article describes novel therapeutic approaches for the treatment of heart failure that target mechanisms responsible for adaptive exercise-induced cardiac remodeling, which are being developed and tested in preclinical models.

引用

页码：515 / +

页数：17

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