Abstract
Embryonic heart progenitors arise at specific spatiotemporal periods that contribute to the formation of distinct cardiac structures. In mammals, the embryonic and fetal heart is hypoxic by comparison to the adult heart. In parallel, the cellular metabolism of the cardiac tissue, including progenitors, undergoes a glycolytic to oxidative switch that contributes to cardiac maturation. While oxidative metabolism is energy efficient, the glycolytic-hypoxic state may serve to maintain cardiac progenitor potential. Consistent with this proposal, the adult epicardium has been shown to contain a reservoir of quiescent cardiac progenitors that are activated in response to heart injury and are hypoxic by comparison to adjacent cardiac tissues. In this review, we discuss the development and potential of the adult epicardium and how this knowledge may provide future therapeutic approaches for cardiac repair.
Highlights
Cardiovascular diseases represent a prevalent medical challenge and are a leading cause of morbidity and mortality in developed societies
We present an overview of the different cell types that participate in mammalian heart development as well as how the microenvironment participates in cardiac remodeling
Significant debate exists regarding the identity and functional potential of adult cardiac progenitor cells (CPCs), there is an emerging consensus that the adult epicardium contains cells with progenitor potential that can participate in cardiac remodeling after injury
Summary
Cardiovascular diseases represent a prevalent medical challenge and are a leading cause of morbidity and mortality in developed societies. It has been proposed that the epicardium secretes mitogenic signals that drive cardiomyocyte proliferation in the compact zone[31,32,33] (Figures 1A, 1B) Another cellular compartment derived from cardiogenic mesoderm SHF consists of specialized endothelial cells (endocardium) that cover the inner surface of the cardiac tube and participate in different heart morphogenesis processes, which include trabeculation and a part of the coronary tree formation[16,34,35,36]. The murine heart undergoes a metabolic switch to oxidative metabolism coupled with the maturation and bi-nucleation of cardiomyocytes, and the maturation of the coronary vasculature, which is driven by the availability of oxygen This raises the hypothesis that low levels of oxygen during early postnatal life present a permissive context in which regeneration can occur.
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