The same underlying molecular and cellular damage of aging contributes to both calcification of blood vessel walls and the development of atherosclerosis, but researchers here argue that calcification can be considered on its own, an independent risk factor for cardiovascular dysfunction and mortality in later life. The presence of senescent cells is one of the common underlying factors that accelerates the progression of both atherosclerosis and calcification of blood vessels. This is due to the inflammatory signaling produced by these cells. That signaling distorts the behavior of macrophages trying to clear up deposits of cholesterol in blood vessel walls, but also makes other cells in the wall behave as though they are osteoblasts in bone, laying down mineral deposits.
molecular and cellular damage of agingcalcification of blood vessel wallsatherosclerosissenescent cellsboth atherosclerosis and calcification of blood vesselsinflammatory signalingmacrophagescholesterolosteoblasts
Calcification, like the creation of cross-links or degradation of elastin in the extracellular matrix, is harmful because it reduces elasticity in blood vessels. That loss of elasticity breaks the feedback mechanisms that control blood pressure, and the result is the development of hypertension. Hypertension causes structural damage throughout the body: small blood vessels rupture at an accelerated rate in the delicate tissues of the brain,
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