In this issue of Cardiovascular Research, Qin et al} show that the incidence of abdominal aortic aneurysm formation in apolipoprotein E (apo E) knockout mice is profoundly inhibited if the mice are additionally deficient in cathepsin S, an elastinolytic cysteine proteinase. Cathepsin S, traditionally thought of as a lysosomal proteinase involved only in the terminal degradation of endocytosed proteins, is now known to be active in the cytosol, the nucleus, and the extracellular matrix and to play a number of diverse cell-specific rotes, including the destruction of extracellular matrix collagen and elastin and weakening of the arterial wall.2'3 Some cells can also release cathepsin S in a regulated manner to facilitate their migration and, in the case of endothelial cells, to allow new blood vessels to invade tissue.
展开▼
