Staubesand J
MMW Munch Med Wochenschr. 1979 Jan 12;121(2):57-62.
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.
损伤因素（如异常的血流动力学和/或代谢状况——“血管壁的危险因素”）导致收缩性（k）平滑肌细胞转变为代谢更活跃或“修饰”（m）的类型，进而导致细胞内和细胞外溶酶体（基质溶酶体）数量增加，最终导致中膜发育异常。随着电子显微镜证实了非典型（即发育异常）的胶原纤维和弹性纤维，作为动脉瘤、静脉曲张等病因的“血管壁薄弱”这一模糊概念已被更精确的描述所取代。血管壁的肌肉细胞似乎会对改变的状况做出反应，增加溶酶体的数量，进而增加溶酶体酶的数量。电子显微镜还揭示了基质溶酶体附近的胶原分解、弹性蛋白分解和蛋白聚糖分解。
