2022
DOI: 10.1016/j.freeradbiomed.2022.05.010
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Mitochondrial and glucose metabolic dysfunctions in granulosa cells induce impaired oocytes of polycystic ovary syndrome through Sirtuin 3

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Cited by 56 publications
(41 citation statements)
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“…Mild oxidative stress induces the expression of SIRTs probably as a compensatory mechanism, while severe or long-lasting oxidant conditions result in decreased SIRT levels due to the generation of dysfunctional modified SIRTs that are more prone to degradation by the proteasome [ 81 ]. In addition, SIRT3 deficiency in granulosa cells of PCOS patients may contribute to mitochondrial dysfunction, elevated oxidative stress, and defects in glucose metabolism, which potentially induce impaired oocytes in PCOS [ 82 ]. Therefore, the correlation between epigenetic factors and ROS generation can also manifest itself the other way around.…”
Section: Oxidative Stress and Inflammatory Signaling In Pcosmentioning
confidence: 99%
“…Mild oxidative stress induces the expression of SIRTs probably as a compensatory mechanism, while severe or long-lasting oxidant conditions result in decreased SIRT levels due to the generation of dysfunctional modified SIRTs that are more prone to degradation by the proteasome [ 81 ]. In addition, SIRT3 deficiency in granulosa cells of PCOS patients may contribute to mitochondrial dysfunction, elevated oxidative stress, and defects in glucose metabolism, which potentially induce impaired oocytes in PCOS [ 82 ]. Therefore, the correlation between epigenetic factors and ROS generation can also manifest itself the other way around.…”
Section: Oxidative Stress and Inflammatory Signaling In Pcosmentioning
confidence: 99%
“…A study found that the decreased expression of mir-181a could inhibit the apoptosis of GCs in vitro and in vivo by upregulating the expression of SIRT1 and the deacetylation of the pro-apoptotic factor FoxO1 (61,62). The expression of Sirtuin 3 (SIRT3) was significantly reduced in GCs of PCOS patients, while the knockdown of SIRT3 could change the acetylation state of NDUFS1, which may induce mitochondrial dysfunction, elevated oxidative stress, and glucose metabolism defects, leading to damage of oocytes in PCOS (63). Protein lysine acetylation is not only found on histones that affect chromatin structure and gene expression, but also on non-histones involved in a variety of cellular processes, thus providing an opportunity to explore the mechanism of acetylation regulation of PCOS as a drug target for the development of new therapies.…”
Section: Acetylationmentioning
confidence: 99%
“…High levels of oxidative stress in the follicular fluid are associated with poor oocyte maturation and embryo quality [26]. Mitochondrial dysfunction that is characterized by high levels of accumulated free radicals is the key cause of oxidative stress and oxidative stress-induced cell aging [27]. Antioxidants such as Melatonin, Coenzyme Q, Vitamins A and E may be crucial for increasing the reproductive capacity by improving mitochondrial function.…”
Section: Antioxidantsmentioning
confidence: 99%