Mitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington School of Medicine, Seattle, WA 98109, USA.
Circ Res. 2013 Aug 16;113(5):603-16. doi: 10.1161/CIRCRESAHA.113.302095.
The network for cardiac fuel metabolism contains intricate sets of interacting pathways that result in both ATP-producing and non-ATP-producing end points for each class of energy substrates. The most salient feature of the network is the metabolic flexibility demonstrated in response to various stimuli, including developmental changes and nutritional status. The heart is also capable of remodeling the metabolic pathways in chronic pathophysiological conditions, which results in modulations of myocardial energetics and contractile function. In a quest to understand the complexity of the cardiac metabolic network, pharmacological and genetic tools have been engaged to manipulate cardiac metabolism in a variety of research models. In concert, a host of therapeutic interventions have been tested clinically to target substrate preference, insulin sensitivity, and mitochondrial function. In addition, the contribution of cellular metabolism to growth, survival, and other signaling pathways through the production of metabolic intermediates has been increasingly noted. In this review, we provide an overview of the cardiac metabolic network and highlight alterations observed in cardiac pathologies as well as strategies used as metabolic therapies in heart failure. Lastly, the ability of metabolic derivatives to intersect growth and survival are also discussed.
心脏燃料代谢网络包含错综复杂的相互作用途径,这些途径为每一类能量底物都产生了产生 ATP 和不产生 ATP 的终点。该网络最显著的特点是表现出对各种刺激的代谢灵活性,包括发育变化和营养状况。心脏还能够在慢性病理生理条件下重塑代谢途径,从而调节心肌能量和收缩功能。为了了解心脏代谢网络的复杂性,人们已经使用药理学和遗传学工具来在各种研究模型中操纵心脏代谢。同时,已经在临床上测试了许多治疗干预措施来针对底物偏好、胰岛素敏感性和线粒体功能。此外,细胞代谢通过产生代谢中间产物对生长、存活和其他信号通路的贡献也越来越受到关注。在这篇综述中,我们概述了心脏代谢网络,并强调了心脏病理学中观察到的变化以及在心力衰竭中作为代谢疗法使用的策略。最后,还讨论了代谢衍生物与生长和存活交叉的能力。