Ca2+ handling alterations and vascular dysfunction in diabetes

• We review alterations of vascular Ca2+ signaling proteins associated with the diabetic condition.
• We emphasize alterations of Ca2+ signaling proteins in diabetic vascular smooth muscle.
• We report gender differences of functional STOC/spark coupling in the diabetic condition.

More than 65% of patients with diabetes mellitus die from cardiovascular disease or stroke. Hyperglycemia, due to either reduced insulin secretion or reduced insulin sensitivity, is the hallmark feature of diabetes mellitus. Vascular dysfunction is a distinctive phenotype found in both types of diabetes and could be responsible for the high incidence of stroke, heart attack, and organ damage in diabetic patients. In addition to well-documented endothelial dysfunction, Ca2+ handling alterations in vascular smooth muscle cells (VSMCs) play a key role in the development and progression of vascular complications in diabetes. VSMCs provide not only structural integrity to the vessels but also control myogenic arterial tone and systemic blood pressure through global and local Ca2+ signaling. The Ca2+ signalosome of VSMCs is integrated by an extensive number of Ca2+ handling proteins (i.e. channels, pumps, exchangers) and related signal transduction components, whose function is modulated by endothelial effectors. This review summarizes recent findings concerning alterations in endothelium and VSMC Ca2+ signaling proteins that may contribute to the vascular dysfunction found in the diabetic condition.

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