Epidemiological Research Advances in Vascular Calcification in Diabetes

Abstract

Vascular calcification is the transformation of arterial wall mesenchymal cells, particularly smooth muscle cells (SMCs), into osteoblast phenotypes by various pathological factors. Additionally, vascular transformation mediates the abnormal deposition of calcium salts in the vascular wall, such as intimal and media calcification. Various pathological types have been described, such as calcification and valve calcification. The incidence of vascular calcification in patients with diabetes is much higher than that in nondiabetic patients, representing a critical cause of cardiovascular events in patients with diabetes. Because basic research on the clinical transformation of vascular calcification has yet to be conducted, this study systematically expounds on the risk factors for vascular calcification, vascular bed differences, sex differences, ethnic differences, diagnosis, severity assessments, and treatments to facilitate the identification of a new entry point for basic research and subsequent clinical transformation regarding vascular calcification and corresponding clinical evaluation strategies.

Dental Diseases Increase Risk of Aortic Arch Calcification Independent of Renal Dysfunction in Older Adults: Shenzhen Community Cohort Study

“…Vascular calcification (VC) is a common and featured arterial pathological condition in chronic kidney disease and diabetes [26,27]. The dental diseases could lead to impaired kidney function [9,28], and are also associated with an increased risk of diabetes [29].…”

Influence of DNA Methylation on Vascular Smooth Muscle Cell Phenotypic Switching

“…Additionally, some specific research demonstrates an association of hyperlipidemia with Wnt/β-catenin signaling, which is crucial in vascular calcification [ 121 , 122 ]. Insulin stimulates the vascular endothelium in order to release nitric oxide, which reduces intimal calcification and inhibits VSMC formation [ 123 ]. However, insulin resistance increases the influx of free fatty acids into the liver, leading to the elevated hepatic uptake of triglycerides and the synthesis of very low-density lipoprotein, thereby increasing the risk of vascular calcification [ 124 ].…”

Molecular Mechanisms Underlying Pathological and Therapeutic Roles of Pericytes in Atherosclerosis

“…VC is characterised as a pathological accumulation of calcium phosphate crystals in the vessel wall or inside of atherosclerosis plaque. As an active and well-orchestrated process, VC shares numerous pathways with normal physiologic bone formation, suggesting a crosstalk between bones and vascular systems [ 69 ]. This process termed as “bone-vascular axis” is mediated through a variety of osteoblast-like cells, which could be derived from other cells: progenitor cells, ECs in the aortic intima, VSMCs in the media, pericytes in the microvessels, myofibroblasts in the adventitia and calcifying vascular cells (CVCs) [reviewed in [ 70 ]].…”