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甲基化circPTK2作为肺纤维化中的纤维细胞激活的驱动因素

Yuguang Zhu¹, Lixin Zhao¹, Jianfeng Qin¹

¹Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA & State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.

Molecular therapy : the journal of the American Society of Gene Therapy

|December 11, 2025

概括

通过激活纤维细胞,circPTK2的N6-甲基氨酸 (m6A) 修饰驱动肺纤维化. 针对这种m6A修饰的circPTK2显示出治疗肺部痕和呼吸衰竭的希望.

科学领域:

分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
在RNA生物学,RNA生物学.

背景情况:

肺纤维化 (PF) 涉及纤维细胞激活和肺部痕.
表观遗传调节,特别是像N6-甲基氨酸 (m6A) 这样的RNA修饰,与PF有关,但尚未完全理解.
循环RNAs (circRNAs) 在PF病变发生中的作用需要进一步研究.

研究的目的:

为了研究m6A修饰的circPTK2在肺纤维化中的作用.
阐明circPTK2有助于纤维细胞激活和PF进展的机制.
评估circPTK2-m+作为PF的潜在治疗标.

主要方法:

在PF患者和模型中识别和描述circPTK2.
评估circPTK2-m+在纤维细胞激活和纤维化中的功能.
研究涉及METTL3,RBMX和EIF4A3.3的m6A修饰途径.
分析circPTK2-m+作为对抗微RNA (miRNA) 的内源RNA (ceRNA) 的分析.

主要成果:

在PF中,circPTK2被上调,其m6A修饰形式 (circPTK2-m+) 驱动纤维细胞激活.
沉默circPTK2-m+或抑制其m6A修饰减弱了体外和体内纤维化.
METTL3和RBMX促进circPTK2-m+的产生,而EIF4A3则促进其核出口.
circPTK2-m+作为ceRNA,隔离miR-484和miR-125a-3p以增强YAP1,FYN和STAT3的激活,促进一个profibrotic程序.

结论:

m6A 修改 circPTK2 是肺纤维化的一个关键驱动因素.
circPTK2-m+通过ceRNA活动促进纤维细胞激活和益纤维细胞转录程序.
circPTK2-m+代表了肺纤维化干预的新且有前途的治疗标.

关键词:

在METTL3中,METTL3是METTL3的第一个类型.这是一种N6-甲基氨酸.在STAT3中,我们可以使用STAT3.环PTK2 环PTK2 环PTK2 环PTK2 纤维细胞激活的激活肺部纤维化肺部纤维化

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