Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, 66421, Homburg, Germany.
Basic Res Cardiol. 2013 Jul;108(4):358. doi: 10.1007/s00395-013-0358-9. Epub 2013 Jun 6.
It has become common sense that the failing heart is an "engine out of fuel". However, undisputable evidence that, indeed, the failing heart is limited by insufficient ATP supply is currently lacking. Over the last couple of years, an increasingly complex picture of mechanisms evolved that suggests that potentially metabolic intermediates and redox state could play the more dominant roles for signaling that eventually results in left ventricular remodeling and contractile dysfunction. In the pathophysiology of heart failure, mitochondria emerge in the crossfire of defective excitation-contraction coupling and increased energetic demand, which may provoke oxidative stress as an important upstream mediator of cardiac remodeling and cell death. Thus, future therapies may be guided towards restoring defective ion homeostasis and mitochondrial redox shifts rather than aiming solely at improving the generation of ATP.
众所周知，衰竭的心脏就像是“没有燃料的引擎”。然而，目前还缺乏确凿的证据表明，衰竭的心脏确实受到了 ATP 供应不足的限制。在过去的几年中，不断涌现出的更为复杂的机制表明，潜在的代谢中间产物和氧化还原状态可能在信号转导中发挥更为重要的作用，最终导致左心室重构和收缩功能障碍。在心力衰竭的病理生理学中，线粒体成为了兴奋-收缩偶联缺陷和能量需求增加的交叉火力点，这可能会引发氧化应激，作为心脏重构和细胞死亡的重要上游介质。因此，未来的治疗方法可能会着眼于恢复异常的离子稳态和线粒体氧化还原状态，而不仅仅是单纯地提高 ATP 的生成。
