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在心肌梗塞后,TRIM44通过TAK1稳定加剧心脏纤维化

Hao Qian¹, Zhengri Lu¹, Chunshu Hao¹

¹Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing 210009, China.

Cellular signalling

|June 4, 2023

概括

通过稳定TAK1.1,TRIM44促进心肌梗塞后的心脏纤维化. 抑制TRIM44在小鼠模型中减少了纤维化,表明TRIM44是心脏病的治疗点.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
纤维化研究纤维化研究

背景情况:

心肌梗塞 (MI) 导致心脏纤维化,这种情况没有有效的治疗方法.
众所周知,TRIM44是一种E3结合酶,可促进瘤细胞的生长和迁移.
在心脏纤维化中TRIM44的作用仍然未被探索.

研究的目的:

研究TRIM44在心脏纤维化中的作用.
阐明TRIM44在纤维化中的作用的潜在分子机制.
评估TRIM44作为心脏纤维化的潜在治疗标.

主要方法:

已建立的小鼠模型的心肌梗塞 (MI) 和TGF-β1诱导的心脏纤维化.
在体内和体外 (心脏纤维细胞) 使用了TRIM44的淘汰和过度表达.
研究了涉及TAK1稳定性,无处不在和MAPK信号传递的机制.

主要成果:

在心脏病发作模型中,TRIM44 knockdown 显著抑制了心脏纤维化.
在心脏纤维细胞和MI模型中,TRIM44过度表达增强了纤维化标志物.
TRIM44通过抑制多基化,激活MAPK和促进纤维化来稳定TAK1.

结论:

TRIM44在促进心脏纤维化方面发挥着至关重要的作用.
TRIM44通过稳定TAK1而起作用,从而导致MAPK的激活.
TRIM44代表了治疗心脏纤维化的有前途的治疗标.

关键词:

心脏纤维化是什么心脏纤维化在心肌梗塞后的心肌梗塞.这就是TAK1的意义.在 TRIM4444 中,在Ubiquitination中使用.

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