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Pediatr Cardiol. 2018 Jun;39(5):1042-1051. doi: 10.1007/s00246-018-1859-y. Epub 2018 Mar 13.

Zinc and Zinc Transporters: Novel Regulators of Ventricular Myocardial Development.

Lin W1,2, Li D3.

Author information

1
Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
2
Regeneron Pharmaceuticals, Inc., Tarrytown, NY, 10591, USA.
3
Division of Cardiac Surgery, School of Medicine, University of Maryland, 800 West Baltimore ST, Rm 314, Baltimore, MD, 21201, USA. dqLi@som.umaryland.edu.

Abstract

Ventricular myocardial development is a well-orchestrated process involving different cardiac structures, multiple signal pathways, and myriad proteins. Dysregulation of this important developmental event can result in cardiomyopathies, such as left ventricle non-compaction, which affect the pediatric population and the adults. Human and mouse studies have shed light upon the etiology of some cardiomyopathy cases and highlighted the contribution of both genetic and environmental factors. However, the regulation of ventricular myocardial development remains incompletely understood. Zinc is an essential trace metal with structural, enzymatic, and signaling function. Perturbation of zinc homeostasis has resulted in developmental and physiological defects including cardiomyopathy. In this review, we summarize several mechanisms by which zinc and zinc transporters can impact the regulation of ventricular myocardial development. Based on our review, we propose that zinc deficiency and mutations of zinc transporters may underlie some cardiomyopathy cases especially those involving ventricular myocardial development defects.

KEYWORDS:

Compaction; Differentiation; ECM; Endocardium; Heart development; LVNC; Myocardium; Proliferation; Signaling pathway; Trabeculation; Zinc; Zip8

PMID:
29536133
DOI:
10.1007/s00246-018-1859-y
[Indexed for MEDLINE]

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