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乙化阅读器BRD4驱动的TXNIP转录增强了PCOS中的NLRP3炎症酶激活

Yajing Weng^1,2, Yi Zhang², Wei Dong²

¹Center for Reproductive Medicine and Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China.

Cellular and molecular life sciences : CMLS

|November 25, 2025

概括

多囊性卵巢综合征 (PCOS) 涉及卵巢颗粒细胞功能障碍. 含有基因的蛋白4 (BRD4) 和雄激素受体 (AR) 调高基因相互作用蛋白 (TXNIP),激活NLRP3炎症体并引起PCOS症状.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
生殖医学生殖医学

背景情况:

多囊卵巢综合征 (PCOS) 是一种常见的内分泌疾病,影响生殖年龄的女性,其特点是颗粒细胞 (GC) 功能障碍和不孕症.
与异常基因素乙化相关的持久性铁素相互作用蛋白 (TXNIP) 激活与PCOS有关,但上游调节者尚不清楚.

研究的目的:

阐明TXNIP在PCOS病原体中的上游调控机制.
在PCOS模型中,研究原体含有蛋白4 (BRD4) 和雄激素受体 (AR) 在TXNIP调节中的作用.

主要方法:

使用了脱氨 (DHEA) 诱导的PCOS类老鼠模型和二氨 (DHT) 诱导的初级GC模型.
使用的TXNIP/NLRP3抑制剂 (ruscogenin),TXNIP向的siRNA,BRD4抑制剂 (JQ1) 和AR抑制剂.
进行了生物信息分析,以确定TXNIP促进体上的转录因子结合基因.

主要成果:

在体内和体外PCOS模型中,TXNIP的调节显著上升.
抑制TXNIP或NLRP3炎症酶激活可以逆转PCOS相关的生殖和代谢异常.
发现BRD4和AR与乙化TXNIP促进体结合,并且它们的抑制降低了TXNIP转录和NLRP3炎症酶激活.

结论:

在PCOS中,BRD4和AR介导的TXNIP转录激活是驱动NLRP3炎症酶激活的关键途径.
针对BRD4/AR/TXNIP轴为PCOS相关的生殖和代谢功能障碍提供了潜在的治疗策略.

关键词:

雄激素受体的受体雄激素受体含有基多马因的蛋白质4 在NLRP3炎症酶体中,NLRP3炎症多囊性卵巢综合征多囊性卵巢综合征铁素相互作用的蛋白质与铁素相互作用

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