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三甲基胺氧化物通过激活JAK2-STAT3通路促进心肌纤维化

Xiaoyun Yang¹, Yi Wang¹, Yujin Feng¹

¹The Department of Abdominal Ultrasound, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China.

Biochemical and biophysical research communications

|January 31, 2025

概括

三甲基胺N氧化物 (TMAO) 通过增加原沉积,显著恶化心肌梗塞后的心脏纤维化. TMAO激活JAK2/STAT3通路,促进心脏纤维细胞激活和纤维化发展.

科学领域:

心血管生物学心血管生物学
分子心脏病学分子心脏病学
纤维化研究纤维化研究

背景情况:

心肌梗塞 (MI) 通常导致心肌纤维化,损害心脏功能.
高水平的三甲基胺N氧化物 (TMAO) 与心血管疾病风险增加有关.

研究的目的:

调查TMAO对心肌梗塞后心脏纤维化发展的直接影响.
阐明涉及TMAO诱导心脏纤维化中的分子机制,特别是JAK/STAT通路.

主要方法:

建立了心肌梗塞的小鼠模型,并用TMAO或不使用TMAO进行治疗.
通过心声学评估心脏功能;使用马森染色量化纤维化.
免疫组织化学和西部斑点分析了 I 和 III 类型的原蛋白,纤维菌素和 JAK / STAT 途径蛋白.
在体外研究中使用了用TMAO和JAK2/STAT3抑制剂 (AG490) 治疗的心脏纤维细胞.

主要成果:

在体内,TMAO的使用显著增加了心脏纤维化,原沉积和纤维素和I和III类原的表达.
在体外,TMAO在心脏纤维细胞中调节了纤维素,原蛋白I和原蛋白III.
通过JAK2/STAT3信号通路的激活,TMAO的亲纤维效应得到了调解.

结论:

在心肌梗塞后,TMAO会加剧心肌纤维化.
TMAO通过JAK2/STAT3通路促进心脏纤维细胞激活和细胞外基质沉积.
准JAK2/STAT3通路可能是缓解TMAO诱导心脏纤维化的治疗策略.

关键词:

JAK2/STAT3 3 的情况.心肌纤维化是心肌纤维化的一种.这就是TMAOO.

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