Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants
Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants
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DOI：
10.1590/s0100-879x2011007500112
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发表时间：
2011-09-01
影响因子：
2.3
通讯作者：
Oliveira, E.M.
中科院分区：
文献类型：
--
作者：
Fernandes, T.;Soci, U.P.R.;Oliveira, E.M.
在响应于生理刺激或病理损伤而协调心脏肥大的不同表型的发展的分子、生物化学和细胞过程中，运动训练的具体贡献最近已被认识到。生理性心脏肥大涉及复杂的心脏重构，其作为对静态或动态慢性运动的适应性反应而发生，但对血液动力学过载转导到心肌生长的刺激和分子机制知之甚少。本文综述了诱导向心性和离心性心肌肥厚的生理刺激，并讨论了其分子机制、肌节结构和信号通路，同时指出病理性心肌肥厚的心肌标志物（心房利钠因子、β-肌球蛋白重链和α-骨骼肌动蛋白）并未增加。离心性或向心性心肌肥厚无纤维化，无心功能障碍。因此，肾素-血管紧张素系统被认为是控制心脏功能和结构的调节机制之一。在这里，我们表明，血管紧张素II 1型（AT 1）受体是局部激活的病理性和生理性心脏肥大，虽然与运动训练，它可以刺激独立的血管紧张素II的参与。最近，microRNAs（miRs）已被研究作为一种可能的治疗方法，因为它们调节参与心脏肥大的靶mRNA的翻译;然而，与生理性肥大相关的miRs尚未被广泛研究。我们在此总结了在病理性和生理性心脏肥大中检测miR的研究概况。了解生理性心脏重构可能为改善心功能不全时的心室功能提供策略。
Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of the hemodynamic overload into myocardial growth are poorly understood. This review summarizes the physiological stimuli that induce concentric and eccentric physiological hypertrophy, and discusses the molecular mechanisms, sarcomeric organization, and signaling pathway involved, also showing that the cardiac markers of pathological hypertrophy (atrial natriuretic factor, beta-myosin heavy chain and alpha-skeletal actin) are not increased. There is no fibrosis and no cardiac dysfunction in eccentric or concentric hypertrophy induced by exercise training. Therefore, the renin-angiotensin system has been implicated as one of the regulatory mechanisms for the control of cardiac function and structure. Here, we show that the angiotensin II type 1 (AT1) receptor is locally activated in pathological and physiological cardiac hypertrophy, although with exercise training it can be stimulated independently of the involvement of angiotensin II. Recently, microRNAs (miRs) have been investigated as a possible therapeutic approach since they regulate the translation of the target mRNAs involved in cardiac hypertrophy; however, miRs in relation to physiological hypertrophy have not been extensively investigated. We summarize here profiling studies that have examined miRs in pathological and physiological cardiac hypertrophy. An understanding of physiological cardiac remodeling may provide a strategy to improve ventricular function in cardiac dysfunction.