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Ovarian follicle atresia

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Ovarian follicle atresia is the periodic process in which immature ovarian follicles degenerate
and are subsequently re-absorbed during the follicular phase of the menstrual cycle. Typically
around 20 follicles mature each month and only a single follicle is ovulated. The rest undergo
atresia. That single dominant follicle becomes a corpus luteumfollowing ovulation.[1][2][3][4]
Atresia is a hormonally controlled apoptotic process[5] that depends dominantly on granulosa cell
apoptosis.
To date, at least five cell-death ligand-receptor systems have been reported in granulosa cells to
play a role in atresia regulation.[6][7][3] They are:

tumor necrosis factor alpha (TNF alpha) and receptors

Fas ligand and receptors[2]

TNF-related apoptosis-inducing ligand (TRAIL; also called APO-2) and receptors

APO-3 ligand and receptors

PFG-5 ligand and receptors

In addition, two intracellular inhibitor proteins, cellular FLICE-like inhibitory protein short form
(cFLIPS) and long form (cFLIPL), which were strongly expressed in granulosa cells, may act as
anti-apoptotic factors.
It has been proposed that enhanced levels of Nitrogen oxide in rats can prevent atresia of the
ovarian follicle, and depressed levels have the opposite effect.[8]

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