ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
IL-22/IL-22R signaling attenuates mitochondrial damage in PCOS by modulating granulosa cell lipid metabolism through ETS1.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study investigates the therapeutic potential of interleukin-22 (IL-22) in polycystic ovary syndrome (PCOS) and its mechanisms.
methodsA dehydroepiandrosterone (DHEA)-induced PCOS mouse model and testosterone-treated human KGN granulosa cells were utilized. Mice received IL-22 (50-100 µg/kg) or Diane-35 for 3 weeks.
resultsIL-22 administration restored estrous cyclicity, reduced ovarian cysts, and normalized serum testosterone and insulin levels in DHEA or letrozole-induced PCOS mice. DHEA induction led to mitochondrial damage in granulosa cells (GCs), evidenced by impaired mitochondrial membrane potential, mtDNA copy number depletion, and ROS accumulation, alongside lipid metabolic dysregulation. These detrimental effects were ameliorated by IL-22. Bioinformatics analysis of PCOS patient data revealed significant enrichment in lipid metabolism pathways. A high-fat diet abolished IL-22's PCOS-restoring effects, underscoring lipid metabolism as a key mechanism. We identified 19 lipid metabolism-related genes, with ETS1 being the most significantly regulated. IL-22 inhibited ETS1 expression induced by DHEA through the activation of STAT3 dependent on the IL-22R1, and Chromatin Immunoprecipitation (ChIP)-PCR confirmed STAT3 binding to the ETS1 promoter.
conclusionOur findings highlight IL-22 as a promising therapeutic candidate for PCOS, acting through the IL-22R1/STAT3/ETS1 pathway to ameliorate mitochondrial dysfunction and lipid metabolic reprogramming in GCs. This study bridges immune signaling with metabolic pathology in PCOS, offering novel avenues for targeted intervention.
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