Diabetes mellitus (DM) is a worldwide growing disease and represents a huge social and healthcare problem owing to the\r\nburden of its complications. Micro- and macrovascular diabetic complications arise from excess damage through well-known\r\nbiochemical pathways. Interestingly, microangiopathy hits the bone marrow (BM) microenvironment with features similar to\r\nretinopathy, nephropathy and neuropathy. TheBMrepresents a reservoir of progenitor cells formultiple lineages, not limited to the\r\nhematopoietic system and including endothelial cells, smoothmuscle cells, cardiomyocytes, and osteogenic cells. All thesemultiple\r\nprogenitor cell lineages are profoundly altered in the setting of diabetes in humans and animal models. Reduction of endothelial\r\nprogenitor cells (EPCs) along with excess smooth muscle progenitor (SMP) and osteoprogenitor cells creates an imbalance that\r\npromote the development of micro- and macroangiopathy. Finally, an excess generation of BM-derived fusogenic cells has been\r\nfound to contribute to diabetic complications in animal models. Taken together, a growing amount of literature attributes to\r\ncirculating progenitor cells a multi-faceted role in the pathophysiology of DM, setting a novel scenario that puts BM and the blood\r\nat the centre of the stage.
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