APOPTOSIS DURING WOUND-HEALING, FIBROCONTRACTIVE DISEASES AND VASCULAR WALL INJURY

Following injury, tissue repair involves information, granulation tiss ue formation and scar constitution. Granulation tissue develops from t he connective tissue surrounding the damaged or missing area and conta ins mainly small vessels, inflammatory cells, fibroblasts and myofibro blasts. As the wound closes and evolves into a scar, there is a striki ng decrease in cellularity, including disappearance of typical myofibr oblasts. The question arises as to what process is responsible for gra nulation tissue cell disappearance. Our results (in cutaneous wounds) and results of other laboratories (particularly in lungs and kidney) s uggest that apoptosis is the mechanism responsible for the evolution o f granulation tissue into a scar. During excessive scarring (hypertrop hic scar or fibrosis), it is conceivable that the process of apoptosis cannot take place. After experimental endothelial injury in an artery , accumulation of smooth muscle cells participates in the formation of intimal thickening. Apoptotic features have been observed in cells of intimal thickening and also within human atherosclerotic plaques. In the case of atherosclerosis, apoptosis could be detrimental: since smo oth muscle cells participate in plaque stability, apoptosis could lead to weakening and rupture of the plaque. These results underline the f act that both increased cell survival or excessive cell death can be a ssociated with pathological disorders. Specific therapies devised to e nhance or decrease the susceptibility of individual cell types to apop tosis development could modify the evolution of a variety of human dis eases. (C) 1997 Elsevier Science Ltd.