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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]
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doi: 10.3389/fphar.2020.00041
Conversely, decreased Cav-1 level or obstructed Cav-1 and eNOS interaction can release eNOS favoring its activation and induction of nitric oxide production that is known for its protective effect on vessels 44,45
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