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=== Related Diseases ===
=== Related Diseases ===
Undergoing follicular atresia is necessary in order for mammals to maintain a healthy reproductive system. However, disorders in the regulation of follicle breakdown and generation can lead to various pathologies:
Undergoing follicular atresia is necessary in order for mammals to maintain a healthy reproductive system. Mammalian ovaries ovulate about 1% of the follicles and the remaining follicles may go through atresia as it cycles through the growth phases.<ref>{{Cite journal |last=Liu |first=Zhenteng |last2=Li |first2=Fenghua |last3=Xue |first3=Jingwen |last4=Wang |first4=Meimei |date=2020 |title=Esculentoside A rescues granulosa cell apoptosis and folliculogenesis in mice with premature ovarian failure |url=https://www.aging-us.com/lookup/doi/10.18632/aging.103609 |journal=Aging |volume=12 |issue=17 |pages=16951–16962 |doi=10.18632/aging.103609 |issn=1945-4589 |pmc=PMC7521512 |pmid=32759462}}</ref> However, disorders in the regulation of follicle breakdown and generation can lead to various pathologies:


==== Premature Ovarian Failure<ref>{{Citation |last=Gago |first=L. April |title=Premature Ovarian Failure |date=2004-01-01 |url=https://www.sciencedirect.com/science/article/pii/B0124755704010660 |work=Encyclopedia of Endocrine Diseases |pages=65–72 |editor-last=Martini |editor-first=Luciano |place=New York |publisher=Elsevier |language=en |isbn=978-0-12-475570-3 |access-date=2022-07-28 |last2=Ginsburg |first2=Kenneth A.}}</ref> ====
==== Premature Ovarian Failure<ref>{{Citation |last=Gago |first=L. April |title=Premature Ovarian Failure |date=2004-01-01 |url=https://www.sciencedirect.com/science/article/pii/B0124755704010660 |work=Encyclopedia of Endocrine Diseases |pages=65–72 |editor-last=Martini |editor-first=Luciano |place=New York |publisher=Elsevier |language=en |isbn=978-0-12-475570-3 |access-date=2022-07-28 |last2=Ginsburg |first2=Kenneth A.}}</ref> ====

Revision as of 05:52, 1 August 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 refers to the process in which a follicle fails to develop, thus preventing it from ovulating and releasing an egg.[3] It is a normal, naturally occurring, progressive process that encompasses 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.[4]Oocytes are then able to mature within the follicle through meiosis. However, 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[5]. Only one follicle will be mature enough to release an egg and may be fertilized[6]. Typically, around 20 follicles mature each month, but only a single follicle is ovulated; the follicle from the oocyte was released becomes the corpus luteum. The corpus luteum is the last stage of the ovarian follicles' lifecycle. It has an important role in secreting estrogen and progesterone to prepare the body for conception. If conception does not occur, then it will be shed and is known as the corpus albicans[7]. It has been observed that this mechanism is important in regulating and maintaining a healthy reproductive system in mammals. It is also a subject of interest in understanding and predicting fertility in female humans.

Mechanism

Atresia is a complex, hormonally controlled apoptotic process that depends dominantly on granulosa cell apoptosis, however there have been other proposed mechanisms in which this pathway occurs. In the most known mechanism, 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: [4][8]

Granulosa cell apoptosis is induced by tumor necrosis factor-alpha (TNFα), although the mechanism of how it occurs is unclear.[9]

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.[10] Lack of a working Fas ligand / Fas receptor system has been linked to abnormal follicle development, and increased secondary follicles as a result of the inability to induce apoptosis.[11]

TNF-related apoptosis-inducing ligand (TRAIL) activates caspase 3 (CASP3), which interacts with caspases 6, 7, 8, 9, and 10, to induce apoptosis in granulosa cells.[12]

In addition, two intracellular inhibitor proteins, cellular FLICE-like inhibitory protein short form (cFLIPS) and long form (cFLIPL), which are strongly expressed in granulosa cells, may act as anti-apoptotic factors.[13]

Anti-Mullerian hormone (AMH) has been studied to be a key regulator in the ovaries in humans that inhibits follicular atresia. Using indirect comparators to derive this hypothesis, exploring different patient populations such as individuals who have polycystic ovary syndrome (PCOS) help support the hypothesis that AMH may be a key regulator in inhibiting follicular atresia. [14]

Menopause

Follicular atresia occurs throughout all stages of follicular development, until the follicular reserve is completely exhausted.[15] Exhaustion of the follicular reserve occurs at menopause, which is typically around the age of 51 in humans with ovaries. The dramatic decrease in estrogen and progesterone levels that is characteristic of menopause, is caused by follicular atresia. Breakdown of the follicles prevent them from releasing hormones such as estrogen. Progesterone levels also decrease during menopause because without any follicles, there is no development of a corpus luteum, which is the major source of circulating progesterone levels in humans.[16]

Studies have shown that follicular atresia does not occur at a constant rate.[15]

Undergoing follicular atresia is necessary in order for mammals to maintain a healthy reproductive system. Mammalian ovaries ovulate about 1% of the follicles and the remaining follicles may go through atresia as it cycles through the growth phases.[17] However, disorders in the regulation of follicle breakdown and generation can lead to various pathologies:

Premature Ovarian Failure[18]

Premature ovarian failure (POF) (also called premature ovarian insufficiency) is the loss of ovarian function before the age of 40 due to follicular dysfunction such as accelerated follicular atresia. There may be many causes of POF, ranging from genetic disorders to surgery, radiation therapy, and exposure to environmental toxicants. Accelerated follicular atresia due to chromosomal and genomic defects accounts for up to one-half of all POF cases. For example, Fragile X syndrome, Turner syndrome, and various autosomal diseases such as galactosemia have been linked to follicular deficiencies. Smoking has also been found to increase follicular atresia and lead to premature ovarian failure.[19]

Ovarian Follicular Cysts[20][21]

When an ovarian follicle fails to undergo atresia and release an egg, it can grow to form a cyst. This may be due to an overproduction of FSH or an inadequate supply of LH. Most follicular cysts are harmless and resolve on their own within several months. However, rarely a cyst will grow to be very large (greater than 7 cm), cause abdominal pain or rupture, or last for longer than a few months, in which case a physician may recommend surgical removal or testing to determine if it is cancerous. Ultrasound is a common method of visualizing a cyst to determine treatment.

Ovarian Cancer

Since FSH inhibits follicular atresia, the overproduction of FSH can lead to excessive follicle formation and increased risk of ovarian cancer. [22]

The inability to regulate granulosa cell apoptosis has been linked to the development of some hormone-related cancers and chemo-resistance.[+orig. citation here]

According to the gonadotropin theory, follicular depletion associated with incessant follicular atresia has also been hypothesized as a potential etiology for ovarian cancer, due to an increase in serum gonadotropins. This leads to an inflammatory environment which promotes cellular turnover and tumor development.[23]

Morphology

From studying dairy cows, two forms of follicular atresia have been identified: antral and basal.

Antral

Antral follicular atresia is characterized by the apoptosis of granulosa cells within the antral layers of the granulosa membrane and sometimes within the antrum itself. During this process, the presence of pyknotic nuclei in the antral layers of the membrane can be observed.[24] Apoptosis ensures that the follicle gets eliminated without triggering an inflammatory response.[25] Antral follicular atresia causes no damage to basal granulosa cells. This type of follicular atresia is often considered the classic and most commonly observed form. In most species, it occurs throughout follicular development and is universally seen in large follicles (>5 mm diameter).[25]

Basal

Basal follicular atresia is characterized by the destruction of granulosa cells in the basal layer of the granulosa membrane. Macrophages have often been observed, penetrating the basal lamina during this type of follicular atresia. These macrophages phagocytose the basal granulosa cells. An increased deposition of collagen in the theca layer of the follicle can also be observed.[24] Basal follicular atresia causes no damage to antral granulosa cells.This form of follicular atresia has only been observed in small follicles of dairy cows (< 5mm diameter), and has not been reported in any other species.[25]

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. ^ McGee, Elizabeth A.; Horne, Jessica (2018), Skinner, Michael K. (ed.), "Follicle Atresia", Encyclopedia of Reproduction (Second Edition), Oxford: Academic Press, pp. 87–91, doi:10.1016/b978-0-12-801238-3.64395-7, ISBN 978-0-12-815145-7, retrieved 2022-07-31
  4. ^ a b 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.
  5. ^ 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)
  6. ^ Zhang, Jinbi; Liu, Yang; Yao, Wang; Li, Qifa; Liu, Honglin; Pan, Zengxiang (2018). "Initiation of follicular atresia: gene networks during early atresia in pig ovaries". Reproduction. 156 (1): 23–33. doi:10.1530/REP-18-0058. ISSN 1741-7899.
  7. ^ Kirkendoll, Shelbie D.; Bacha, Dhouha (2022), "Histology, Corpus Albicans", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31424854, retrieved 2022-07-26
  8. ^ Torres-Ramirez, N (2019). Endoplasmic Reticulum Stress during Mammalian Follicular Atresia. IntechOpen. ISBN 9781838800888.
  9. ^ 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)
  10. ^ 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.
  11. ^ Porter, D. A.; Harman, R. M.; Cowan, R. G.; Quirk, S. M. (2001). "Relationship of Fas ligand expression and atresia during bovine follicle development". Reproduction (Cambridge, England). 121 (4): 561–566. ISSN 1470-1626. PMID 11277875.
  12. ^ Naimi, Adel; Movassaghpour, Ali Akbar; Hagh, Majid Farshdousti (2018). "TNF-related apoptosis-inducing ligand (TRAIL) as the potential therapeutic target in hematological malignancies". Biomedicine & Pharmacotherapy. 98: 566–576. doi:10.1016/j.biopha.2017.12.082. ISSN 0753-3322.
  13. ^ Manabe, Noboru; Goto, Yasufumi; Matsuda-Minehata, Fuko; Inoue, Naoko (2004). "Regulation Mechanism of Selective Atresia in Porcine Follicles: Regulation of Granulosa Cell Apoptosis during Atresia". Journal of Reproduction and Development. 50 (5): 493–514. doi:10.1262/jrd.50.493. ISSN 0916-8818.
  14. ^ Seifer, David B.; Merhi, Zaher (2014). "Is AMH a regulator of follicular atresia?". Journal of Assisted Reproduction and Genetics. 31 (11): 1403–1407. doi:10.1007/s10815-014-0328-7. ISSN 1058-0468. PMC 4389943. PMID 25193290.
  15. ^ a b Banerjee, Sayani; Banerjee, Sutapa; Saraswat, Ghungroo; Bandyopadhyay, Soma Aditya; Kabir, Syed N. (2014). "Female Reproductive Aging Is Master-Planned at the Level of Ovary". PLoS ONE. 9 (5): e96210. doi:10.1371/journal.pone.0096210. ISSN 1932-6203. PMC 4008600. PMID 24788203.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  16. ^ Gore, Andrea C. (2003), Aminoff, Michael J.; Daroff, Robert B. (eds.), "Women's Health, Neurology of", Encyclopedia of the Neurological Sciences, New York: Academic Press, pp. 763–766, doi:10.1016/b0-12-226870-9/01136-9, ISBN 978-0-12-226870-0, retrieved 2022-08-01
  17. ^ Liu, Zhenteng; Li, Fenghua; Xue, Jingwen; Wang, Meimei (2020). "Esculentoside A rescues granulosa cell apoptosis and folliculogenesis in mice with premature ovarian failure". Aging. 12 (17): 16951–16962. doi:10.18632/aging.103609. ISSN 1945-4589. PMC 7521512. PMID 32759462.{{cite journal}}: CS1 maint: PMC format (link)
  18. ^ Gago, L. April; Ginsburg, Kenneth A. (2004-01-01), Martini, Luciano (ed.), "Premature Ovarian Failure", Encyclopedia of Endocrine Diseases, New York: Elsevier, pp. 65–72, ISBN 978-0-12-475570-3, retrieved 2022-07-28
  19. ^ Klinger, Francesca G.; Rossi, Valerio; De Felici, Massimo (2015). "Multifaceted programmed cell death in the mammalian fetal ovary". The International Journal of Developmental Biology. 59 (1–3): 51–54. doi:10.1387/ijdb.150063fk. ISSN 1696-3547. PMID 26374525.
  20. ^ Cole, Laurence; Kramer, Peter R. (2016-01-01), Cole, Laurence; Kramer, Peter R. (eds.), "Chapter 6.8 - Ovarian Cystic Disorders", Human Physiology, Biochemistry and Basic Medicine, Boston: Academic Press, pp. 219–221, ISBN 978-0-12-803699-0, retrieved 2022-07-28
  21. ^ "Follicular Cyst | Definition & Patient Education". Healthline. 2016-09-23. Retrieved 2022-07-28.
  22. ^ Zhang, Zhenbo; Jia, Lin; Feng, Youji; Zheng, Wenxin (2009-06-08). "Overexpression of follicle-stimulating hormone receptor facilitates the development of ovarian epithelial cancer". Cancer Letters. 278 (1): 56–64. doi:10.1016/j.canlet.2008.12.024. ISSN 0304-3835.
  23. ^ Smith, Elizabeth R; Xu, Xiang-Xi (2008). "Ovarian ageing, follicle depletion, and cancer: a hypothesis for the aetiology of epithelial ovarian cancer involving follicle depletion". The lancet oncology. 9 (11): 1108–1111. doi:10.1016/S1470-2045(08)70281-X. ISSN 1470-2045. PMC 2713057. PMID 19012860.
  24. ^ a b Makarevich, Alexander V.; Földešiová, Martina; Pivko, Juraj; Kubovičová, Elena; Chrenek, Peter (2018). "Histological characteristics of ovarian follicle atresia in dairy cows with different milk production". Anatomia, Histologia, Embryologia. 47 (6): 510–516. doi:10.1111/ahe.12389.
  25. ^ a b c H., David; M.H., Catherine (2012), Darwish, Atef (ed.), "Ovarian Follicular Atresia", Basic Gynecology - Some Related Issues, InTech, doi:10.5772/32465, ISBN 978-953-51-0166-6, retrieved 2022-07-26
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