YAP O-GlcNAcylation 在暴露于香烟烟雾的情况下,有助于角膜上皮细胞铁亡
Meng-Yuan Zhang1, Ting-Ting Wei2, Cheng Han1
1Department of Ophthalmology, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, China.
Environmental pollution (Barking, Essex : 1987)
|August 18, 2024
概括
香烟烟雾 (CS) 通过铁亡诱导角膜细胞死亡,这是一种涉及铁的积累和脂质过氧化的过程. 抑制YAP稳定,这是该途径的关键因素,可以防止CS诱导的眼睛表面损伤.
科学领域:
- 眼科医生 眼科 眼科
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 香烟烟雾 (CS) 是一个重要的室内空气污染物,与眼睛表面疾病有关.
- 视角膜,眼睛的外层,特别容易受到空气污染物,如CS.
- 将CS暴露与角膜功能障碍联系在一起的机制需要进一步阐明.
研究的目的:
- 调查CS引发角膜上皮细胞损伤的分子机制.
- 为了确定关键的途径和分子点参与CS诱导的眼表面功能障碍.
- 探索潜在的治疗策略,以减轻CS相关的眼睛疾病.
主要方法:
- 角膜上皮细胞中CS暴露模型.
- 评估细胞活力,铁含量和脂质过氧化.
- 对铁灭菌标记物和相关蛋白质表达的分析 (TFRC,ACSL4,YAP).
- 通过O-GlcNAcylation和ubiquitination对YAP调节的研究.
- 对关键分子标的药理和遗传抑制.
主要成果:
- CS暴露导致角膜上皮细胞损伤,其特征是铁和脂质过氧化增加,表明铁亡.
- CS上调调节了TFRC和ACSL4的表达,促进了铁的吸收和脂质过氧化.
- 抑制TFRC或ACSL4可以预防CS诱导的铁亡.
- YAP转录的上调驱动了TFRC和ACSL4的表达.
- CS暴露增加了O-GlcNAc转移酶活性,导致YAP O-GlcNAcylation和稳定,从而促进铁亡.
- 抑制YAP或其O-GlcNAcylation保护的角膜细胞免受CS诱导的损伤.
结论:
- CS通过涉及YAP O-GlcNAcylation和随后的稳定的途径诱导角膜上皮细胞铁亡.
- 准YAP O-GlcNAcylation路径为CS诱导的眼睛表面疾病提供了潜在的治疗策略.
- CS暴露是确诊的眼球表面疾病的风险因素,通过角膜细胞中的铁死介导.
关键词:
香烟烟雾的烟雾是什么意思视角膜 视角膜 是一个铁性化 (ferroptosis) 是一种这是一种O-GlcNAcylation.哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈更多相关视频
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