Abstract
Decline in circulating sex steroid hormones accompanies several age-associated pathologies which may influence human healthspan. Mitochondria play important roles in biosynthesis of sex steroid hormones, and these hormones can also regulate mitochondrial function. Understanding the cross talk between mitochondria and sex steroid hormones may provide insights into the pathologies associated with aging. The aim of this review is to summarize the current knowledge regarding the interplay between mitochondria and sex steroid hormones during the aging process. The review describes the effect of mitochondria on sex steroid hormone production in the gonads, and then enumerates the contribution of sex steroid hormones on mitochondrial function in hormone responsive cells. Decline in sex steroid hormones and accumulation of mitochondrial damage may create a positive feedback loop that contributes to the progressive degeneration in tissue function during aging. The review further speculates whether regulation between mitochondrial function and sex steroid hormone action can potentially influence healthspan.
Highlights
Sex steroid hormones play important roles in maintaining normal reproductive and non-reproductive functions
Because aging is accompanied by decreasing levels of circulating sex steroid hormones [1,2], many researchers and clinicians had previously hypothesized that the decline in these hormones promotes tissue degeneration and age-related pathologies
This review summarizes the current knowledge regarding the crosstalk between mitochondria and sex steroid hormones during aging, and examines whether the interplay between mitochondrial function and sex steroid hormone action can potentially influence healthspan
Summary
Sex steroid hormones play important roles in maintaining normal reproductive and non-reproductive functions. Continuous ovulation and follicular atresia, plus inability of follicles to naturally regenerate, eventually lead to reduced sex steroid hormone production Aside from this progressive decline in follicle numbers, it is suggested that excessive oxidative damage in the ovaries, due to a decrease in the levels of antioxidants, may be a potential contributing factor for reproductive aging [54]. This suggests that while estrogen can protect normal cells from oxidative stress, it exacerbates oxidative stress in damaged cells, that is, cancer cells While it remains unclear what mechanisms regulate this contradictory effect of estrogen on mitochondrial ROS production, the contribution of damaged versus healthy cell on estrogen action is consistent with the critical window and healthy cell hypothesis of estrogen replacement therapy [22,100]. While estrogen can directly and indirectly regulate mitochondrial biogenesis and function, it remains to be confirmed whether testosterone can significantly contribute to mitochondrial function
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