Molecular basis of reproductive senescence: insights from model organisms
- PMID: 33006069
- PMCID: PMC7822982
- DOI: 10.1007/s10815-020-01959-4
Molecular basis of reproductive senescence: insights from model organisms
Abstract
Purpose: Reproductive decline due to parental age has become a major barrier to fertility as couples have delayed having offspring into their thirties and forties. Advanced parental age is also associated with increased incidence of neurological and cardiovascular disease in offspring. Thus, elucidating the etiology of reproductive decline is of clinical importance.
Methods: Deciphering the underlying processes that drive reproductive decline is particularly challenging in women in whom a discrete oocyte pool is established during embryogenesis and may remain dormant for tens of years. Instead, our understanding of the processes that drive reproductive senescence has emerged from studies in model organisms, both vertebrate and invertebrate, that are the focus of this literature review.
Conclusions: Studies of reproductive aging in model organisms not only have revealed the detrimental cellular changes that occur with age but also are helping identify major regulator proteins controlling them. Here, we discuss what we have learned from model organisms with respect to the molecular mechanisms that maintain both genome integrity and oocyte quality.
Keywords: Aging; Cohesion; DNA damage; Nondisjunction; Oocyte quality; Proteostasis.
Conflict of interest statement
The authors declare that they have no conflict of interest.
References
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- Roeters van Lennep JE, Heida KY, Bots ML, Hoek A, collaborators of the Dutch Multidisciplinary Guideline Development Group on Cardiovascular Risk Management after Reproductive D Cardiovascular disease risk in women with premature ovarian insufficiency: a systematic review and meta-analysis. Eur J Prev Cardiol. 2016;23(2):178–186. doi: 10.1177/2047487314556004. - DOI - PubMed
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