Abstract
Rationale: Therapeutic potential of c-Kit+ cardiac progenitor cells (CPCs) is modest in autologous cell therapy clinical trials and could benefit from optimization to maximize functional activity. Early proliferation arrest limits expansion potential of human CPCs in vitro. In contrast, self-renewal is preserved and mitochondrial reactive oxidative species (mtROS) minimized within the CPC hypoxic niche in vivo. Expansion under oxygen tension comparable to the hypoxic niche may therefore improve CPC reparative function.
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