Rimbaud Stéphanie, Garnier Anne, Ventura-Clapier Renée
INSERM, U-769, Châtenay-Malabry, France.
Pharmacol Rep. 2009 Jan-Feb;61(1):131-8. doi: 10.1016/s1734-1140(09)70015-5.
Cardiac performance depends on a fine balance between the work the heart has to perform to satisfy the needs of the body and the energy that it is able to produce. Thus, energy production by oxidative metabolism, the main energy source of the cardiac muscle, has to be strictly regulated to adapt to cardiac work. Mitochondrial biogenesis is the mechanism responsible for mitochondrial component synthesis and assembly. This process controls mitochondrial content and thus correlates with energy production that, in turn, sustains cardiac contractility. Mitochondrial biogenesis should be finely controlled to match cardiac growth and cardiac work. When the heart is subjected to an increase in work in response to physiological and pathological challenges, it adapts by increasing its mass and expressing a new genetic program. In response to physiological stimuli such as endurance training, mitochondrial biogenesis seems to follow a program involving increased cardiac mass. But in the context of pathological hypertrophy, the modifications of this mechanism remain unclear. What appears clear is that mitochondrial biogenesis is altered in heart failure, and the imbalance between cardiac work demand and energy production represents a major factor in the development of heart failure.
心脏功能取决于心脏为满足身体需求而必须完成的工作与它能够产生的能量之间的精确平衡。因此，作为心肌主要能量来源的氧化代谢产生能量的过程必须受到严格调控，以适应心脏工作。线粒体生物合成是负责线粒体成分合成与组装的机制。这一过程控制线粒体含量，进而与维持心脏收缩力的能量产生相关。线粒体生物合成应得到精细调控，以匹配心脏生长和心脏工作。当心脏因生理和病理挑战而工作负荷增加时，它会通过增加质量和表达新的基因程序来适应。响应耐力训练等生理刺激时，线粒体生物合成似乎遵循一个涉及心脏质量增加的程序。但在病理性肥大的情况下，该机制的改变仍不清楚。显而易见的是，心力衰竭时线粒体生物合成会发生改变，心脏工作需求与能量产生之间的失衡是心力衰竭发展的一个主要因素。
