OOCYTE AGING: GENETICS AND EPIGENETICS OF EGG QUALITY
“๐๐ ๐๐ช๐ฅ๐ ๐๐๐๐๐ ๐๐ค ๐๐ฃ๐๐ง๐๐, ๐๐ฅ ๐๐๐๐ค๐ฅ ๐๐ ๐ก๐๐ฃ๐ฅ, ๐๐ช ๐๐๐๐ฆ๐๐ฆ๐๐๐ฅ๐๐ ๐๐๐๐๐๐ ๐ฅ๐ ๐ปโ๐ธ, ๐๐๐๐๐ฆ๐๐๐๐ ๐๐ ๐ฆ๐๐๐-๐ค๐ฅ๐ฃ๐๐๐ ๐๐ฃ๐๐๐๐ค ๐ฅ๐๐๐ฅ ๐ฅ๐๐ ๐ ๐ ๐๐ช๐ฅ๐’๐ค ๐ฃ๐๐ก๐๐๐ฃ ๐๐๐๐๐๐๐๐ฃ๐ช ๐๐๐๐ ๐๐๐ค ๐๐๐๐ฃ๐๐๐ค๐๐๐๐๐ช ๐ฆ๐๐๐๐๐ ๐ฅ๐ ๐๐๐ฉ ๐ ๐ง๐๐ฃ ๐ฅ๐๐๐.” - Prof. Jonathan Tilly
๐งฌ Oocyte aging is central to the decline in female fertility. Both genetic damage and epigenetic drift impair egg quality, embryonic development, and overall reproductive potential.
๐น With age, oocytes accumulate DNA damage. Genes such as BRCA1 and RAD51, vital for DNA double-strand break repair, show reduced expression, leading to increased aneuploidy (abnormal number of chromosomes). Variants in genes like FSHR also affect ovarian responsiveness and egg quality.
๐น Aging disrupts DNA methylation and histone modifications essential for gene expression during oocyte maturation. Environmental exposures and oxidative stress accelerate this disruption. Interventions using antioxidants (CoQ10, vitamins C & E) may help restore mitochondrial and epigenetic integrity.
๐น Genetic and epigenetic changes are deeply interwoven; mutations may promote epigenetic instability, while faulty epigenetic regulation impairs gene expression. Emerging tools like CRISPR/Cas9 -based epigenome editing provide new avenues to improve egg quality and fertility outcomes.
⚠️ In an Oystershell, as more women delay childbirth, understanding and mitigating oocyte aging becomes urgent. Integrated genetic–epigenetic insights are essential for personalized fertility strategies and improved assisted reproduction outcomes.
Abubakar Abubakar ✍๐ป
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