Molecular basis of reproductive senescence: insights from model organisms
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REVIEW
Molecular basis of reproductive senescence: insights from model organisms Cristina Quesada-Candela 1 & Julia Loose 2 & Arjumand Ghazi 2 & Judith L. Yanowitz 1 Received: 17 August 2020 / Accepted: 25 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
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 . Nondisjunction . Oocyte quality . Proteostasis . Cohesion . DNA damage
Introduction Over the last 30 years, we have seen the average age at first conception increase by > 3.5 years as women delay childbearing. More and more couples suffer from infertility associated with maternal and paternal age. While assisted reproductive technologies (ART) offer increasing alternatives for men and women to bank reproductive cells and tissues, these technologies do not come without risks, including increased likelihood of imprinting disorders and failure to implant. ART also depends on the ability to procure healthy egg and sperm, and in cases of premature ovarian failure (POF) and advanced maternal age, this is often not feasible. POF is itself associated * Judith L. Yanowitz [email protected]; https://orcid.org/0000-0001-68868787 1
Magee-Womens Research Institute, Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh School of Medicine, 204 Craft Avenue, Pittsburgh, PA 15213, USA
2
Departments of Pediatrics, Developmental Biology and Cell Biology and Physiology, John G. Rangos Sr. Research Center, University of Pittsburgh School of Medicine, Room 7129, One Children’s Hospital Drive, 4401 Penn Avenue, Pittsburgh, PA 15224, USA
with increased risk for metabolic and cardiovascular disorders [1] that have led to the question of whether reproductive decline is itself driving deterioration of somatic tissues. Furthermore, reproductive decline is the earliest manifestations of aging experienced by most organisms and thus insight into i
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