Arterial Calcification in Diabetes Mellitus: Preclinical Models and Translational Implications.

摘要: Diabetes mellitus increasingly afflicts our aging and dysmetabolic population. Type 2 diabetes the antecedent metabolic syndrome represent vast majority of disease burden-increasingly prevalent in children older adults. However, type 1 is also advancing preadolescent children. As such, a crushing wave cardiometabolic burden now faces society. Arteriosclerotic calcification increased syndrome, mellitus, mellitus-impairing conduit vessel compliance function, thereby increasing risk for dementia, stroke, heart attack, limb ischemia, renal insufficiency, lower extremity amputation. Preclinical models these settings have provided insights into pathobiology arterial calcification. Osteochondrogenic morphogens BMP-Wnt signaling relay transcriptional regulatory programs driven by Msx Runx gene families are entrained to innate immune responses-responses activated state-to direct matrix deposition mineralization. Recent studies implicate endothelial-mesenchymal transition contributing phenotypic drift mineralizing vascular progenitors. In this brief overview, we discuss preclinical that provide mechanistic insights-and point challenges opportunities translate new therapeutic strategies patients afflicted with its arteriosclerotic complications.