Abstract：
Copper is an essential trace metal element that significantly affects human physiology and pathology by regulating various important biological processes, including mitochondrial oxidative phosphorylation, iron mobilization, connective tissue crosslinking, antioxidant defense, melanin synthesis, blood clotting, and neuron peptide maturation. Increasing lines of evidence obtained from studies of cell culture, animals, and human genetics have demonstrated that dysregulation of copper metabolism causes heart disease, which is the leading cause of mortality in the US. Defects of copper homeostasis caused by perturbed regulation of copper chaperones or copper transporters or by copper deficiency resulted in various types of heart disease, including cardiac hypertrophy, heart failure, ischemic heart disease, and diabetes mellitus cardiomyopathy. This review aims to provide a timely summary of the effects of defective copper homeostasis on heart disease and discuss potential underlying molecular mechanisms.
摘要：
铜是一种必需的痕量金属元素，通过调节各种重要的生物过程而显著影响人体生理和病理，包括线粒体氧化磷酸化，铁动员，结缔组织交联，抗氧化防御，黑色素合成，血液凝固,和神经元肽成熟。从细胞培养研究中获得的证据越来越多，动物,人类遗传学已经证明铜代谢失调会导致心脏病，这是美国死亡的主要原因。铜分子伴侣或铜转运蛋白的调节紊乱或铜缺乏引起的铜稳态缺陷导致各种类型的心脏病，包括心脏肥大,心力衰竭,缺血性心脏病,和糖尿病心肌病。本文旨在及时总结铜稳态缺陷对心脏病的影响，并讨论潜在的潜在分子机制。
