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=== Overview ===
=== Overview ===
'''Follicular atresia''' is the breakdown of the [[ovarian follicles]] which are made in mammalian ovaries in order to secrete hormones and oocytes. Oocytes are immature eggs and are surrounded by [[granulosa cells]] and internal and external [[theca]] cells.<ref name=":0">{{Cite journal |last=Zhou |first=Jiawei |last2=Peng |first2=Xianwen |last3=Mei |first3=Shuqi |date=2019 |title=Autophagy in Ovarian Follicular Development and Atresia |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6429023/ |journal=International Journal of Biological Sciences |volume=15 |issue=4 |pages=726–737 |doi=10.7150/ijbs.30369 |issn=1449-2288 |pmc=6429023 |pmid=30906205}}</ref> In female humans, this process occurs continuously, as they are born with a finite number of follicles (between 500,000-1,000,000 follicles), and about 99% of follicles undergo atresia<ref>{{Cite journal |last=Wilkosz |first=Pawel |last2=Greggains |first2=Gareth D. |last3=Tanbo |first3=Tom G. |last4=Fedorcsak |first4=Peter |date=2014 |title=Female Reproductive Decline Is Determined by Remaining Ovarian Reserve and Age |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195570/ |journal=PLoS ONE |volume=9 |issue=10 |pages=e108343 |doi=10.1371/journal.pone.0108343 |issn=1932-6203 |pmc=4195570 |pmid=25310678}}</ref>. It has been observed that this mechanism is important in regulating and maintaining a healthy reproductive system in mammals.
'''Follicular atresia''' is the breakdown of the [[ovarian follicles]] which are made in mammalian ovaries in order to secrete hormones and oocytes. Oocytes are immature eggs and are surrounded by [[granulosa cells]] and internal and external [[theca]] cells.<ref name=":0">{{Cite journal |last=Zhou |first=Jiawei |last2=Peng |first2=Xianwen |last3=Mei |first3=Shuqi |date=2019 |title=Autophagy in Ovarian Follicular Development and Atresia |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6429023/ |journal=International Journal of Biological Sciences |volume=15 |issue=4 |pages=726–737 |doi=10.7150/ijbs.30369 |issn=1449-2288 |pmc=6429023 |pmid=30906205}}</ref>Oocytes are then able to mature within the follicle through meiosis. In female humans, this process occurs continuously, as they are born with a finite number of follicles (between 500,000-1,000,000 follicles), and about 99% of follicles undergo atresia<ref>{{Cite journal |last=Wilkosz |first=Pawel |last2=Greggains |first2=Gareth D. |last3=Tanbo |first3=Tom G. |last4=Fedorcsak |first4=Peter |date=2014 |title=Female Reproductive Decline Is Determined by Remaining Ovarian Reserve and Age |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195570/ |journal=PLoS ONE |volume=9 |issue=10 |pages=e108343 |doi=10.1371/journal.pone.0108343 |issn=1932-6203 |pmc=4195570 |pmid=25310678}}</ref>. It has been observed that this mechanism is important in regulating and maintaining a healthy reproductive system in mammals.


=== Mechanism ===
=== Mechanism ===

Revision as of 19:42, 26 July 2022

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.[1][2]

Article Draft

Overview

Follicular atresia is the breakdown of the ovarian follicles which are made in mammalian ovaries in order to secrete hormones and oocytes. Oocytes are immature eggs and are surrounded by granulosa cells and internal and external theca cells.[3]Oocytes are then able to mature within the follicle through meiosis. In female humans, this process occurs continuously, as they are born with a finite number of follicles (between 500,000-1,000,000 follicles), and about 99% of follicles undergo atresia[4]. It has been observed that this mechanism is important in regulating and maintaining a healthy reproductive system in mammals.

Mechanism

Atresia is a complex, hormonally controlled apoptotic process that depends dominantly on granulosa cell apoptosis. Follicular atresia is inhibited by follicle-stimulating hormone (FSH), which promotes follicle development. Once the follicle has developed, it secretes estrogen, which in high levels decreases secretions of FSH. Granulosa cell apoptosis is considered the underlying mechanism of follicular atresia, and has been associated with five ligand-receptor systems involved in cell death: [5]

Granulosa cell apoptosis is induced by tumor necrosis factor-alpha (TNFα), although the mechanism of how it occurs is unclear.[6]

Fas antigen, a cell surface receptor protein, is expressed on granulosa cells and helps mediate signals that induce apoptosis by binding Fas ligand and therefore plays an important role in follicular atresia.[7] Lack of a functional Fas ligand / Fas receptor system has been linked to abnormal follicle development, and greater numbers of secondary follicles as a result of the inability to induce apoptosis.

TNF-related apoptosis-inducing ligand (TRAIL) activates Caspase 3 (CASP3), which in turn interacts with caspases 6, 7, 8, 9, and 10 to induce apoptosis in granulosa cells.

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.

References

  1. ^ Najati, Vahid; Ilkhanipour, Minoo; Salehi, Shahpar; Sadeghi-Hashjin, Goudarz (2008). "Role of nitric oxide on the generation of atretic follicles in the rat ovaries". Pakistan journal of biological sciences: PJBS. 11 (2): 250–254. doi:10.3923/pjbs.2008.250.254. ISSN 1028-8880. PMID 18817198.
  2. ^ Luo, Yuxin; Zhu, Yanbin; Basang, Wangdui; Wang, Xin; Li, Chunjin; Zhou, Xu (2021). "Roles of Nitric Oxide in the Regulation of Reproduction: A Review". Frontiers in Endocrinology. 12: 752410. doi:10.3389/fendo.2021.752410. ISSN 1664-2392. PMC 8640491. PMID 34867795.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Zhou, Jiawei; Peng, Xianwen; Mei, Shuqi (2019). "Autophagy in Ovarian Follicular Development and Atresia". International Journal of Biological Sciences. 15 (4): 726–737. doi:10.7150/ijbs.30369. ISSN 1449-2288. PMC 6429023. PMID 30906205.
  4. ^ Wilkosz, Pawel; Greggains, Gareth D.; Tanbo, Tom G.; Fedorcsak, Peter (2014). "Female Reproductive Decline Is Determined by Remaining Ovarian Reserve and Age". PLoS ONE. 9 (10): e108343. doi:10.1371/journal.pone.0108343. ISSN 1932-6203. PMC 4195570. PMID 25310678.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  5. ^ Zhou, Jiawei; Peng, Xianwen; Mei, Shuqi (2019-01-29). "Autophagy in Ovarian Follicular Development and Atresia". International Journal of Biological Sciences. 15 (4): 726–737. doi:10.7150/ijbs.30369. ISSN 1449-2288. PMC 6429023. PMID 30906205.
  6. ^ Yamamoto, Yuri; Kuwahara, Akira; Taniguchi, Yuka (2015). "Tumor necrosis factor alpha inhibits ovulation and induces granulosa cell death in rat ovaries". Reproductive Medicine and Biology. 14 (3): 107–115. doi:10.1007/s12522-014-0201-5. PMC 4490172. PMID 26161038.{{cite journal}}: CS1 maint: PMC format (link)
  7. ^ Yang, Runjun; Xu, Shangzhong; Zhao, Zhihui; Li, Junya (2012). "Fas ligand expression and mediated activation of an apoptosis program in bovine follicular granulosa cells". Gene. 493 (1): 148–154. doi:10.1016/j.gene.2011.11.032.