Bone marrow (BM) holds a pool of stem and progenitor cells whose role is not limited to hematopoiesis. Indeed,
growing evidences showed that BM-derived progenitors could contribute to various extents to cardiovascular homeostasis.
Notably, diabetic patients experience an intrinsic defect of the progenitor pool, whereas some recent works point directly to an
intrinsic defect of the BM, resulting in defective mobilization and impaired functions of progenitors. These defects could have
important pathophysiological roles in the development of diabetic complications. An integrated approach, which enhances
mobilization of progenitors and improves their functions, could represent a novel method to improve cardiovascular repair by
endogenous progenitors. Furthermore, potential clinical trials of cell therapy would gain benefit from stratagems that enhance
the number and functions of progenitors prior to transplantation. In this review we discuss the strategies to stimulate the mobilization
of progenitors in diabetes and the protocols to improve their functions.