Facundo Heberty di Tarso Fernandes, Brainard Robert Eli, Caldas Francisco Rodrigo de Lemos, Lucas Aline Maria Brito
Faculdade de Medicina, Universidade Federal do Cariri, Barbalha, Brazil.
Valencia College Orlando, Florida, USA.
Adv Exp Med Biol. 2017;982:203-226. doi: 10.1007/978-3-319-55330-6_11.
Cardiac tissue responds to long-term hemodynamic load through initiation of a hypertrophic remodeling program. Importantly, if not counteracted this response will eventually lead to organ failure. Cardiac hypertrophic adaptations are complex, and involve multiple cellular events and the mechanisms underlying the development of cardiac hypertrophy are not well understood. Mitochondrial dysfunction has been indicated as a potential and important player in the development of cardiac hypertrophy. Additionally, substantial evidence shows that a significant portion of mitochondrial processes, necessary for normal cardiomyocyte physiology, are impacted by these hypertrophic changes. In this chapter, we will present and discuss the adaptations and changes in the mitochondrial electron transport system, mitochondrial metabolism, mitochondrial biogenesis, oxidative stress, the opening of the mitochondrial permeability transition pore following hypertrophic stimuli, as well as, review the various drugs (targeting mitochondria) that can be used in treatment of cardiac hypertrophy.
心脏组织通过启动肥厚性重塑程序来应对长期的血流动力学负荷。重要的是，如果这种反应不被抵消，最终将导致器官衰竭。心脏肥厚适应性变化很复杂，涉及多个细胞事件，且心脏肥大发生的潜在机制尚未完全明确。线粒体功能障碍被认为是心脏肥大发展过程中的一个潜在且重要的因素。此外，大量证据表明，正常心肌细胞生理功能所必需的大部分线粒体过程都受到这些肥厚性变化的影响。在本章中，我们将阐述并讨论肥厚性刺激后线粒体电子传递系统、线粒体代谢、线粒体生物发生、氧化应激、线粒体通透性转换孔开放的适应性变化，以及综述可用于治疗心脏肥大的各种（靶向线粒体的）药物。
