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doi:10.1177/039463201202500123 138
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EPCs contribute to postnatal vasculogenesis, and are recruited from the bone marrow to sites of injury via growth factors, cytokines and hypoxia-related signaling pathways, where they differentiate into mature endothelial cells and incorporate themselves into sites of active neovascularization [41, 51]
However, the high correlation between ferroptosis and lipid ROS production suggests that the inhibition of ferroptosis may be an important target for DCM prevention and treatment
