Initial Lesions of Vascular Aging Disease (Arteriosclerosis)

Abstract

Background: In contrast to the well-known morphologic lesions of arteriosclerosis, the initial changes of the disease are less obvious. Commonly, functional disturbances of the endothelium, endothelial dysfunction, are suggested. On the other hand the significance of age-dependent changes in the extracellular matrix with their important role in vessel wall permeability and other features associated with arteriosclerosis should not be overlooked. New topics deal with possible infectious factors, the genetic basis of the disease and the particularities of the unstable atheroma. Objective: Alterations in nitric monoxide and endothelin-1 balance of the endothelium are the key events in the initiation of arteriosclerosis induced by oxidized lipoproteins, cigarette smoking and endotoxin. This frequently supposed mechanism contrasts with earlier opinions on the primary alterations in glycosaminoglycan metabolism and other components of the extracellular matrix against atherogenic factors like hypertension, stress and physical inactivity. Based on a survey of the literature and our own experimental experiences, these changes in connection with the morphometrically determined age-conditioned increase in vascular wall thickness and the above-mentioned new topics on arteriosclerosis were analyzed. Conclusion: The initial lesions of arteriosclerosis starting in youth seem to be fundamentally different from those beginning in old age. The first step in the development of fatty streaks in the arteries of young people is endothelial dysfunction with a decreased formation of nitric monoxide and an increased expression of adhesion molecules. In comparison the genesis of arteriosclerosis in advanced age is characterized by metabolic changes in the endothelium combined with age-conditioned alterations in the extracellular matrix resulting in faster progression of the disease in old age. The multicausal genesis of arteriosclerosis cannot be doubted even if cooperation with infectious factors cannot be excluded. The histopathologic peculiarities of unstable atheroma are described.

Effects of hypertension and ovariectomy on rat hepatocytes. Are amlodipine and lacidipine protective? (A stereological and histological study)

“…Aging, an inevitable situation for all living organisms, is also associated with inflammatory processes. The aging process causes many problems, such as deregulation of normal bodily functions, which leads to many chronic disorders, such as damage to the vascular endothelium or atherosclerosis, and will often produce hypertension (16,17). Old age combined with hypertension may increase the risk of hypertension-related complications (18).…”

Kidneys in Oriental and Occidental Medicine

“…Aging is considered as kidney deficiency. In other words, aging is characterized by the immune, neural and endocrine dysfunctions mentioned above, such as diabetes mellitus, anorexia, hypobulia [22], cognitive dysfunction [23,24,25], hypertension [26], osteoporosis [25], alopecia [27] and chill [28], in addition to arteriosclerosis [29] resulting from slight inflammation [30]. In summary, the concept of the kidney in Oriental medicine is broader than that in Occidental medicine.…”

Matrix Metalloproteinases and Atherogenesis in Dependence of Age

“…Many important new insights were obtained by means of cell cultures after experimental ligature or balloon angioplasty as well as in animals with gene deficiencies or gene transfer. In initial AS, a matrix alteration, presumably induced by a MMPs dysregulation, is to be supposed probably combined with changes in permeability, an activation of macrophages and an increased SMC migration [12,46,69,125] . These lesions turn into a protracted developing arterial intima widening as an early AS phenomenon.…”

“…A qualitative change in the vascular ECM is known, especially an increase of the sulfated glycosaminoglycans in initial AS and plaques with calcinosis whereas a PG decrease is present in atheromatous and fibrous lesions [46] . In early stages of human AS, an increased expression of versican was detectable [9] , but in experimental AS an accumulation of biglycan and perlecan [47] .…”