[A new concept of the pathogenesis of medial dysplasia (author's transl)].
A unifying concept may be set out briefly in the following manner: injurious agents (such as abnormal hemodynamic and/or metabolic conditions--"risk factors for the vessel wall") leads to the transformation of contractile (k) smooth muscle cells into the metabolically more active or "modified" (m) variety leads to an increase in the number of intracellular and extracellular lysosomes (matrix lysosomes) leads to medial dysplasia. The vague concept of a "vessel wall weakness" as the cause of aneurysms, varicose veins etc. has given place to a more precise picture, following the E. M. demonstration of atypical (i.e. dysplastic) collagen fibrils and elastic fibres. The muscle cells of the vessel wall appear to react to the altered conditions with an icrease of lysosomes, and therefore of lysosomal enzymes. The E. M. has also revealed collagenolysis, elastolysis and proteoglycanolysis in the vicinity of matrix lysosomes.
D000818:Animals; D008247:Lysosomes / Q000201:enzymology; D009130:Muscle, Smooth / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D051381:Rats; D014652:Vascular Diseases / Q000209:etiology* / Q000473:pathology
Ein neuer Aspekt zur Pathogenese der Mediadysplasie: Myozytentransformation, Matrix Vesikel und extrazelluläre Lysosomen in der Wand fehlbelasteter Blutgefässe.