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.
Highlights
Metabolism in Heart Disease.Despite decades of efforts to understand its pathogenesis, heart disease remains a leading cause of mortality and places a growing burden on healthcare systems worldwide.Copper is an essential trace metal micronutrient that has been previously overlooked, but has recently gained attention and become an emerging player in the development of heart disease
We thoroughly summarize current knowledge about the roles of copper-dependent enzymes, copper transporters/chaperones, and copper deficiency in heart diseases, including cardiac hypertrophy, heart failure (HF), ischemic heart disease (IHD), and diabetes mellitus (DM) cardiomyopathy, focusing on detailing the molecular mechanisms and providing both preclinical and clinical evidence
Heart disease results in immense health and economic burdens worldwide, and its cause and underlying molecular mechanism must be urgently elucidated
Summary
Copper is an essential trace metal micronutrient that has been previously overlooked, but has recently gained attention and become an emerging player in the development of heart disease. It is less abundant than other metals such as iron and zinc, copper is widely utilized as a catalytic or structural cofactor by enzymes and proteins that are highly relevant to cardiac physiology and pathology. These copper-binding proteins include cytochrome c oxidase (CCO), superoxide dismutase (SOD), metallothionein (MT), ceruloplasmin (CP), and lysyl oxidase (LOX), which regulate mitochondrial respiration, antioxidant defense, iron metabolism, and connective tissue crosslinking [1]. Increasing evidence has demonstrated that dysregulation of copper homeostasis causes heart disease
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