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<Article>
<Journal>
				<PublisherName>University of Sistan and Baluchestan &amp; the Iranian Genetics Society</PublisherName>
				<JournalTitle>Journal of Epigenetics</JournalTitle>
				<Issn>2676-4350</Issn>
				<Volume>7</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>04</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Mitochondria‑targeted antioxidant MitoQ10 ameliorates p-ASK1 and TRAF2/6 in PCOS mouse model</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>8</FirstPage>
			<LastPage>13</LastPage>
			<ELocationID EIdType="pii">9695</ELocationID>
			
<ELocationID EIdType="doi">10.22111/jep.2026.53949.1101</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Ayob</FirstName>
					<LastName>Jabari</LastName>
<Affiliation>Department of Obstetrics and Gynecology, Molud Infertility Center, Zahedan University of Medical Sciences, Zahedan, Iran.</Affiliation>

</Author>
<Author>
					<FirstName>Elnaz</FirstName>
					<LastName>Salahi</LastName>
<Affiliation>Department of Obstetrics and Gynecology, Molud Infertility
Center, Zahedan University of Medical Sciences, Zahedan, Iran.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>11</Month>
					<Day>24</Day>
				</PubDate>
			</History>
		<Abstract>Mitochondrial dysfunction and the resulting oxidative stress have been increasingly recognized as playing a significant role in the development and progression of polycystic ovary syndrome (PCOS), which is the most prevalent endocrine disorder affecting women during their reproductive years. This study was designed to explore the potential therapeutic effects of MitoQ10, a novel antioxidant specifically targeted to the mitochondria, on mitochondrial function and oxidative stress markers in a mouse model of PCOS.&lt;br /&gt;We focused on examining the expression levels of phosphorylated apoptosis signal-regulating kinase 1 (p-ASK1) and tumor necrosis factor receptor-associated factors 2 and 6 (TRAF2/6) in granulosa cells (GCs) obtained from a dehydroepiandrosterone (DHEA)-induced PCOS mouse model by Real-Time PCR and Western blot. Female BALB/c mice were randomly assigned to one of three experimental groups: a Control group, a PCOS group induced by DHEA, and a PCOS + MitoQ10 (500 μmol/L) group. All groups were treated for a duration of 21 days.&lt;br /&gt;The results of our study revealed that the expression levels of p-ASK1, TRAF2, and TRAF6 were significantly elevated in the PCOS group compared to the control group, indicating increased oxidative stress and inflammatory signaling in the PCOS model. Importantly, treatment with MitoQ10 resulted in a downregulation of these elevated expression levels (p ˂ 0.05), suggesting a mitigating effect of MitoQ10 on oxidative stress. However, it was noted that TRAF6 gene expression did not show a statistically significant difference between the MitoQ10-treated group and the PCOS group, indicating a potentially more complex regulatory mechanism for TRAF6.&lt;br /&gt;In conclusion, these preliminary findings provide evidence suggesting that MitoQ10, a readily available dietary supplement, holds promise as a potential effective adjunct in the treatment of PCOS. The observed beneficial effects warrant further investigation through properly designed clinical trials.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">PCOS</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">DHEA</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">MitoQ10</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">p-ASK1</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">TRAF2/6</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Oxidative Stress</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jep.usb.ac.ir/article_9695_33c27f13651f1ff5bb906ba2bb757d22.pdf</ArchiveCopySource>
</Article>
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