Vascular with an increase in osteogenic proteins 4.

Vascular calcification (VC) is the deposition of hydroxyapatite (HA) crystals in the vasculature. It is considered as a bad clinical outcome and a predictor of cardiovascular adverse events 1. It is one of the mechanisms involved in arterial remodeling which refers to a multitude of structural and functional changes in the vascular wall 2. The process of VC is highly similar to physiological mineralization however it occurs in soft tissues (kidney, articular cartilage, cardiovascular tissues) rather than hard ones (bone, cartilage, dentin) 3.VC is complex and involves the trans-differentiation of vascular smooth muscle cells (VSMC) into osteo/chondrocyte like cells associated with an increase in osteogenic proteins 4. It occurs due to the loss of coordination between stimulatory and inhibitory factors including chemical compounds, enzymes, and proteins (discussed later) 1.Of the various tissues vulnerable to ectopic calcification, VC is the most worrying considered as a complexity leading to increased morbidity and mortality associated with cardiovascular diseases 5.
Individuals with particular conditions are greatly prone to develop soft tissue calcification including elderly, individuals with specific life style aspects, metabolic or hormonal disorders, or with genetic diseases 2.VSMC in advanced aged individuals increase the expression of senescence markers ‘prelamin A’ involved in DNA damage and disrupting mitosis favoring VC 6. Moreover, exogenous excessive generation and inhalation of free radicals from cigarette smoking induce oxidative stress, the process greatly associated with cardiovascular disease 7. Hyperglycemia also induces oxidative and osmotic stress activating vascular inflammatory cells and inducing VSMC trans-differentiation. A major contributor of VC pathology is hyperphosphatemia in patients with chronic kidney disease (CKD) as considered a great risk factor of calcium accumulation in vessel wall, in addition increased parathyroid hormone (PTH) in patients with CKD inhibit osteoprotegerin (OPG), main osteoprotective factor 8. Hypervitamosis D is associated with extensive arterial calcium phosphate deposit and upregulation of proteins regulating mineralization9. Mutation in the gene encoding fibroblast growth factor-23 (FGF-23) contribute to VC in CKD patients as it functions in the inhibition of tubular phosphate reabsorption 8. Moreover, calcification is a hallmark of patients with genetic diseases, including, Keutel syndrome, Psedoxanthoma elasticum (PXE) and PXE-like syndrome 2.


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