Abstract
Vascular calcification, which involves the deposition of calcifying particles within the arterial wall, is mediated by atherosclerosis, vascular smooth muscle cell osteoblastic changes, adventitial mesenchymal stem cell osteoblastic differentiation, and insufficiency of the calcification inhibitors. Recent observations implied a role for mesenchymal stem cells and endothelial progenitor cells in vascular calcification. Mesenchymal stem cells reside in the bone marrow and the adventitial layer of arteries. Endothelial progenitor cells that originate from the bone marrow are an important mechanism for repairing injured endothelial cells. Mesenchymal stem cells may differentiate osteogenically by inflammation or by specific stimuli, which can activate calcification. However, the bioactive substances secreted from mesenchymal stem cells have been shown to mitigate vascular calcification by suppressing inflammation, bone morphogenetic protein 2, and the Wingless-INT signal. Vitamin D deficiency may contribute to vascular calcification. Vitamin D supplement has been used to modulate the osteoblastic differentiation of mesenchymal stem cells and to lessen vascular injury by stimulating adhesion and migration of endothelial progenitor cells. This narrative review clarifies the role of mesenchymal stem cells and the possible role of vitamin D in the mechanisms of vascular calcification.
Highlights
Vascular calcification, which involves the deposition of calcifying particles within the endothelial layer or smooth muscle within the medial layer, is an important issue due to its associated complications, such as peripheral arterial occlusive disease and coronary artery disease [1,2,3]
In patients with end-stage renal disease, endothelial progenitor cells (EPCs) with surface markers of CD34+/CD133−/KDR+/CD45− were activated by active vitamin D, which lowered the expression of osteocalcin [79]
Vascular calcification involves the deposition of calcifying particles within the endothelial and the medial layers after vascular damage
Summary
Vascular calcification, which involves the deposition of calcifying particles within the endothelial layer or smooth muscle within the medial layer, is an important issue due to its associated complications, such as peripheral arterial occlusive disease and coronary artery disease [1,2,3]. Vascular calcification is a predictor of overall mortality and poor arteriovenous graft maturation in patients with CKD [7,8]. As these risk factors can influence the endothelial layer and the smooth muscle cells simultaneously, measures to prevent them are vital. Mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) were considered important for the development of vascular calcification. They could be classified as bone marrow derived MSCs or pericytes based on their origin [9] Following their activation by inflammation or specific stimuli, they may differentiate osteogenically, which can activate calcification. This review explains a possible role of MSCs and EPCs in the mechanisms of vascular calcification and a possible role of vitamin D in that mechanism
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