[Mechanism, regulation, and manipulations of follicular atresia]

In ovaries of mammals, an intense loss of germinal cells occurs by follicular atresia throughout the life. In atretic antral follicles, granulosa cells stop proliferating and become apoptotic. Main effectors of apoptosis are caspases which are activated by two ways in granulosa cells, the one involving Fas/TNF-alpha receptor, the other involving factors of the bel-2 family. Atresia is triggered when some essential factors supporting follicular development are lacking. Particularly, terminal follicular development is strictly dependent upon gonadotropin (FSH, then LH in the final preovulatory stage) supply, but factors acting in a paracrine way (growth factors, cytokines, steroids, constituents of extracellular matrix) play also important roles in amplifying gonadotropin action in follicular cells. Some pathological situations such as premature ovarian failure would result from accelerated follicular atresia, triggered by interactions between follicular cells and cells of the immune system. Current methods to control atresia consist in administrating exogenous gonadotropins, or indirectly increasing endogenous gonadotropins, or increasing follicular cell responsiveness to gonadotropins.