[Ovarian apoptosis]

Apoptosis, or programmed cell-dead is one of the main mechanisms in the process of tissular loss. This is an active process of cellular depletion that participates in a direct manner in tissular homeostasis during the life span. This apoptotic process is a key event on the pathology of tumors development. The nature of apoptosis is genetic, but it is triggered by external factors. The caspases are been mentioned as responsible of the specific cellular lost, which is the final outcome. The equilibrium between proliferation and cellular death is determined by a balance of survival factors and death promoters such as genic regulators, hormones, cytokines and growth factors among others. In the ovary, apoptosis regulates follicular proliferation and differentiation. During embryogenesis the magnitude of the population of oogonias is mediated by apoptosis. During the ovarian cycle, apoptosis participates also in the follicular atresia process. It is probable that apoptosis is participating also directly in the accelerated follicular atresia. This mechanism has been hypothesized to be involved in the pathophysiology of premature ovarian failure. The role of apoptosis is some reproductive pathological events such as chronic anovulation, low ovarian reserve and early ovarian dysfunction is still not known. The knowledge of the role of apoptosis in such pathological conditions will contribute to the understanding of the ovarian physiology and will permit to intervene early during the natural history of the disease.