Type 2 diabetes mellitus (T2DM) is a world epidemic with a high prevalence and mortality. The origin of macro and microvascular complications associated with T2DM is complex and new mechanisms to explain their development are emerging. The changes induced by T2DM in the microenvironment of bone marrow (BM) alter the expansion and differentiation of stem cells and have been related to the development of micro and macrovascular diseases. Alterations in the differentiation and function of hematopoietic, endothelial, and mesenchymal stem cells in T2DM patients reduced the mobility of BM stem cells to the circulation and some immature, dysfunctional, or inflammatory cells pass to the blood (mobilopathy). Consequently, tissue repair is impaired, and the tissue damage caused by hyperglycemia, oxidative stress, and inflammation is increased. These alterations can contribute to diabetic complications, decreasing the quality of life, and increasing mortality. The modulation of the bone marrow microenvironment may be a therapeutic target for treating T2DM and its complications. This article analyses the changes induced in BM and their impact on the development of cardiovascular and kidney complications in T2DM. Also, different therapeutic strategies to restore the bone marrow microenvironment and function through the modulation of oxidative stress, inflammation, and adipogenicity are discussed, considering bone marrow as a novel potential therapeutic target to treat vascular complications of diabetes.
Keywords: Type 2 diabetes; bone fragility; bone marrow; cardiovascular disease; diabetic nephropathy; stem cells; therapeutic strategies.
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