The biology of ageing arteries. An integrated view

It is suggested that damaged arterial smooth muscle cells (SMC) and altered structural proteins are interpreted as foreign and degraded by the complement system and by macrophages. At the same time growth factors are liberated, stimulating hyperplasia of SMC. In atheromata this proliferation may be monoclonal. The long-lived proteins in the ground substance are glucosylated by Amadori reactions leading to virtually stable compounds and to polymerization. This process is enhanced by high blood sugar and possibly by vitamin B6 deficiency. The proteoglycans adsorb lipoproteins which are transported to macrophages during the reconstruction of the wall. The combined result of all these changes is a thickened and stiff intima with decreased nutritional flow to the cells and decreased transmissibility of macrophages and other cells. In addition to antihyperlipemic treatment, arteriosclerosis prevention should include antihypertensive treatment preferably with calcium blocking or beta blocking agents or both and antidiabetic treatment, but also nutritional measures including the supply of Mg, Vitamins E and B6 and possibly nitrites.