Progenitor cells mobilized from the bone marrow are recruited to ischemic tissues and increase neovascularization. Cell therapy is a promising new therapeutic option for treating patients with ischemic disorders. The efficiency of cell therapy to augment recovery after ischemia depends on the sufficient recruitment and engraftment of the cells to the target tissue. Homing to sites of active neovascularization is a complex process depending on a timely and spatially orchestrated interplay between chemokines, chemokine receptors, adhesion molecules (selectins and integrins), and intracellular signaling cascades, including also oxidative signaling. This review will focus on the homing mechanisms of progenitor and stem cells to ischemic tissues. Specifically, we discuss the role of chemokines and adhesion molecules such as selectins and integrins and the crosstalk between chemokines and integrins in progenitor cell homing.
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