Influence of the Ovarian Reserve and Oocyte Quality on Livestock Fertility

Singh, Ajay Kumar; Kumar, S. Lava; Beniwal, Rohit; Mohanty, Aradhana; Kushwaha, Bhawna; Rao, H.B.D. Prasada

doi:10.1007/978-3-031-21630-5_4

Cited by 2 publications

(3 citation statements)

References 221 publications

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“…Ultimately, at menopause, the number of remaining follicles drops below 1,000, indicating that ovarian reserve dictates the reproductive lifespan in females 9, 10, 12 . This pattern of oocyte attrition is not exclusive to humans and is conserved across different species 8 . While the loss of germ cells is ongoing throughout a female’s life, significant loss occurs with early oocytes called primordial and primary follicles 4, 10 .…”

Section: Introductionmentioning

confidence: 94%

“…Throughout a female's reproductive lifespan, regulated cell death mechanisms play fundamental roles at various stages of ovarian development, like follicle formation, development, ovulation, and eliminating damaged oocytes [1][2][3][4][5][6][7][8] . For example, in humans, the number of oocytes follows a continuous decreasing trend from a peak of 6-7 million oocytes at 20 weeks of gestation to less than 1 million at birth.…”

Section: Introductionmentioning

confidence: 99%

“…While the loss of germ cells is ongoing throughout a female’s life, significant loss occurs with early oocytes called primordial and primary follicles 4, 10 . It is widely acknowledged that oocyte apoptotic cell death processes cause atresia in primordial and primary follicles via the DNA damage response pathway (DDR) 8, 14 . DDR in early oocytes before birth resembles that observed in somatic cells.…”

Section: Introductionmentioning

confidence: 99%

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Cathepsin B regulates ovarian reserve quality and quantity via mitophagy by modulating IGF1R turnover

Mohanty,

Kumari,

Kumar. S

et al. 2024

Preprint

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The quality and quantity of the ovarian reserve are meticulously regulated through various cell death pathways to guarantee the availability of high-quality oocytes for fertilization. While apoptosis is recognized for contributing to maintaining ovarian reserve, the involvement of other cell death pathways remains unclear. Employing chemical genetics and proteomics, this study reveals the crucial involvement of Cathepsin B in maintaining the ovarian reserve. Results indicate that apoptosis and autophagy play pivotal roles, and inhibiting these pathways significantly increases follicle numbers. Proteomics reveals a dynamic shift from apoptosis to autophagy during follicular development, with Cathepsin B emerging as a key player in this transition. Inhibiting Cathepsin B not only mimics the augmented oocyte reserve observed with autophagy inhibition but also upregulated IGF1R and AKT-mTOR pathways without compromising fertility. Further, IGF1R inhibition partially compromised the protective effects of Cathepsin B inhibition on oocyte reserves, suggesting their interdependence. This association is further supported by the finding that Cathepsin B can degrade IGF1R in vitro. Moreover, the increased IGF1R levels enhance the oocyte mitochondrial membrane potential via transcriptional regulation of mitochondrial biogenesis and mitophagy genes. Remarkably, this Cathepsin B-dependent ovarian reserve maintenance mechanism is conserved in higher-order vertebrates. Cumulatively, our study sheds valuable light on the intricate interplay of autophagy, Cathepsin B, and growth factors in ovarian reserve maintenance, offering potential implications for fertility research.

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Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cathepsin B regulates ovarian reserve quality and quantity via mitophagy by modulating IGF1R turnover

Mohanty,

Kumari,

Kumar. S

et al. 2024

Preprint

Self Cite

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Autophagy and Female Fertility: Mechanisms, Clinical Implications, and Emerging Therapies

Harrath,

Rahman,

Bhajan

et al. 2024

Cells

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Autophagy, an evolutionarily conserved cellular mechanism essential for maintaining internal stability, plays a crucial function in female reproductive ability. In this review, we discuss the complex interplay between autophagy and several facets of female reproductive health, encompassing pregnancy, ovarian functions, gynecologic malignancies, endometriosis, and infertility. Existing research emphasizes the crucial significance of autophagy in embryo implantation, specifically in the endometrium, highlighting its necessity in ensuring proper fetal development. Although some knowledge has been gained, there is still a lack of research on the specific molecular impacts of autophagy on the quality of oocytes, the growth of follicles, and general reproductive health. Autophagy plays a role in the maturation, quality, and development of oocytes. It is also involved in reproductive aging, contributing to reductions in reproductive function that occur with age. This review explores the physiological functions of autophagy in the female reproductive system, its participation in reproductive toxicity, and its important connections with the endometrium and embryo. In addition, this study investigates the possibility of emerging treatment approaches that aim to modify autophagy, using both natural substances and synthetic molecules, to improve female fertility and reproductive outcomes. Additionally, this review intends to inspire future exploration into the intricate role of autophagy in female reproductive health by reviewing recent studies and pinpointing areas where current knowledge is lacking. Subsequent investigations should prioritize the conversion of these discoveries into practical uses in the medical field, which could potentially result in groundbreaking therapies for infertility and other difficulties related to reproduction. Therefore, gaining a comprehensive understanding of the many effects of autophagy on female fertility would not only further the field of reproductive biology but also open new possibilities for diagnostic and treatment methods.

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Influence of the Ovarian Reserve and Oocyte Quality on Livestock Fertility

Cited by 2 publications

References 221 publications

Cathepsin B regulates ovarian reserve quality and quantity via mitophagy by modulating IGF1R turnover

Cathepsin B regulates ovarian reserve quality and quantity via mitophagy by modulating IGF1R turnover

Autophagy and Female Fertility: Mechanisms, Clinical Implications, and Emerging Therapies

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