Potential long-term risks associated with maternal aging (the role of the mitochondria)

Wilding, Martin

doi:10.1016/j.fertnstert.2015.03.034

Cited by 21 publications

(11 citation statements)

References 55 publications

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“…An impressive multi-faceted study of the mechanisms underlying age-related declines in fertility showed that dietary supplementation with CoQ not only reversed the decline in mitochondrial function in the oocytes of ageing female mice, but also increased the numbers of oocytes that these older mice ovulated and restored litter sizes to those produced by young mice [121] (figure 3). The impaired mitochondrial efficiency in oocytes from older females has also been proposed as a mechanism underlying the Lansing effect, if the offspring of older mothers were to inherit a greater proportion of dysfunctional mitochondria which would then shorten their lives [133].…”

Section: (C) Mitochondrial Ageing In the Germlinementioning

confidence: 99%

The deteriorating soma and the indispensable germline: gamete senescence and offspring fitness

2019

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The idea that there is an impenetrable barrier that separates the germline and soma has shaped much thinking in evolutionary biology and in many other disciplines. However, recent research has revealed that the so-called ‘Weismann Barrier’ is leaky, and that information is transferred from soma to germline. Moreover, the germline itself is now known to age, and to be influenced by an age-related deterioration of the soma that houses and protects it. This could reduce the likelihood of successful reproduction by old individuals, but also lead to long-term deleterious consequences for any offspring that they do produce (including a shortened lifespan). Here, we review the evidence from a diverse and multidisciplinary literature for senescence in the germline and its consequences; we also examine the underlying mechanisms responsible, emphasizing changes in mutation rate, telomere loss, and impaired mitochondrial function in gametes. We consider the effect on life-history evolution, particularly reproductive scheduling and mate choice. Throughout, we draw attention to unresolved issues, new questions to consider, and areas where more research is needed. We also highlight the need for a more comparative approach that would reveal the diversity of processes that organisms have evolved to slow or halt age-related germline deterioration.

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Section: (C) Mitochondrial Ageing In the Germlinementioning

confidence: 99%

The deteriorating soma and the indispensable germline: gamete senescence and offspring fitness

2019

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“…A suggested strategy of mitochondrial targeting using nanoparticles may be helpful to resume proper functioning of dysfunctional mitochondria. © 1996-2016 difficulties in the descendants that could be due to the transmission of damaged mtDNA that commonly arise in later life (13)(14)(15)(16). All these studies have now made clear that genetic predisposition could lead to dysfunction of the mitochondrial respiratory chain and may gives rise to heterogeneous group of mitochondrial disorders.…”

Section: Figurementioning

confidence: 99%

“…However, in the process of evolutionary transformation the ability to synthesize most of the proteins encoded by the primitive bacterial DNA were severely abrogated (2). Apart from a small circular polycystronic 16 Kb mtDNA controlling the synthesis of about 67 proteins, including 13 polypeptides of the ETC; the rest were relocated into nuclear genome architecture. During this regulatory transitional stage of adaptability between high and low oxidative rates, mitochondria conserved a few bacterial phenotypic characteristics and acquired many exciting functions.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial anomalies driver to age associated degenerative human ailments

et al. 2016

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Mitochondria play a fundamental role in regulating a variety of complex metabolic processes to maintain adequate energy balance for cellular existence. To orchestrate these functions, an undisturbed mitochondrial dynamics is imperative through a set of tightly guided mechanisms. Interference in key signature processes by several genetic, epigenetic and age-linked factors triggers mitochondrial dysfunction through decrease in mitochondrial biogenesis, reduced mitochondrial content, aberrant mtDNA mutations, increased oxidative stress, deficient mitophagy, energy dysfunction, decrease in anti oxidant defense and impaired calcium homeostasis. Mitochondrial dysfunction is widely implicated in origin and development of various age associated degenerative human ailments including metabolic syndromes, cardiovascular diseases, cancer, diabetes and neurodegenerative disorders. The present review revisits the mitochondrial anomalies involved in aetiology of different human diseases and also highlights the translational significance of nano-vectors aimed for selective mitochondrial engineering which might pave way for development of novel therapeutics.

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“…It is well understood that the rate of pregnancy decreases significantly with the deterioration of oocytes due to aging [4,5]. With aging, oocytes exhibit abnormal chromosome division, decreased mitochondrial quality, including the accumulation of mutations in the mitochondrial DNA and low ATP production, increased oxidative stress, and decreased levels of antioxidants [5][6][7]. We previously demonstrated that the functional characteristics of the bovine oviduct and uterus change with agedependent upregulation of inflammation [3,8].…”

Section: Introductionmentioning

confidence: 99%

Adverse reproductive effects of S100A9 on bovine sperm and early embryonic development in vitro

Funeshima

Tanikawa

Yaginuma³

et al. 2020

PLoS ONE

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The phenomenon of aging arises from multiple, complex interactions causing dysfunction in cells and organs. In particular, fertility drastically decreases with age. Previously, we have demonstrated that the functional characteristics of the bovine oviduct and uterus change with the age-dependent upregulation of inflammation and noted that S100A9 triggers inflammatory responses in oviduct epithelial cells. In the present study, we investigated the hypothesis that S100A9 affects reproductive events to aspect such as sperm function, fertilization, and the development of the embryo in cows. To investigate the effect of S100A9 on bovine sperm, we incubated sperms in vitro with S100A9 for 5 h and observed significantly decreased sperm motility and viability. During in vitro fertilization, S100A9 treatment for 5 h did not affect the rate of fertilization, time of first division of embryos, or embryo development to blastocyst stage. Treatment of 2-cell stage embryos with S100A9 for 5 h significantly reduced the proportion of cells undergoing normal division (4-8 cell embryos) and embryo development to the blastocyst stage. In experiment involving 24 h treatment of 2-cell embryos, the development of all embryos stopped at the 2-cell stage in the S100A9-treated group. In blastocyst-stage embryos, S100A9 treatment significantly stimulated the expression of endoplasmic reticulum (ER) and the mRNA expression of ER stress markers, and activated caspase-3 with subsequent nuclear fragmentation. Pre-treatment with an ER stress inhibitor significantly suppressed caspase-3 activation by the S100A9 treatment, suggesting that S100A9 induces blastocyst dysfunction by apoptosis (via caspase-3 activation) depending on ER stress. These results indicate that direct exposure to S100A9 exerted adverse effects on sperm function and embryo development. These findings suggest that excessive dose of S100A9 may have an adverse effect to the reproductive machinery by inducing inflammation and tissue dysfunction. Adverse reproductive effects of S100A9 on bovine sperm and early embryonic development in vitro. PLoS ONE 15(1): e0227885. https://doi.org/ 10.

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Potential long-term risks associated with maternal aging (the role of the mitochondria)

Cited by 21 publications

References 55 publications

The deteriorating soma and the indispensable germline: gamete senescence and offspring fitness

The deteriorating soma and the indispensable germline: gamete senescence and offspring fitness

Mitochondrial anomalies driver to age associated degenerative human ailments

Adverse reproductive effects of S100A9 on bovine sperm and early embryonic development in vitro

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