血清响应因子在老化大动脉中的活性下降与动脉瘤进展有关
Catarina Rippe1, Joakim Armstrong Bastrup2, Johan Holmberg1
1Vascular Physiology Environment, Department of Experimental Medical Science, Lund University, Lund, Sweden.
The Journal of biological chemistry
|March 13, 2025
概括
衰老的动脉显示了actomyosin成分的减少,影响了收缩性. 在小鼠中,血清反应因子 (SRF) 枯竭模仿与年龄相关的变化,导致大动脉扩大,但可以防止高血压引起的动脉瘤.
科学领域:
- 血管生物学 血管生物学
- 衰老研究研究 衰老研究
- 分子心脏病学分子心脏病学
背景情况:
- 年龄是动脉动脉瘤等动脉疾病的关键因素.
- 衰老的动脉表现出改变的基因表达,特别是与actomyosin相关的转录.
研究的目的:
- 为了研究衰老对人类动脉转录组的影响.
- 阐明血清响应因子 (SRF) 在与年龄相关的动脉变化和大关节病的作用.
主要方法:
- 人体动脉的RNA测序以确定年龄相关的转录变化.
- 在年轻小鼠 (i8-SRF-KO) 中条件删除SRF,以研究其孤立的影响.
- 蛋白质组分析以比较缺少Srf的小鼠与接受血管新生素II (AngII) 治疗的小鼠.
主要成果:
- 衰老的动脉显示了与减少的SRF相关的压抑的actomyosin转录 (MYLK,ACTG2).
- 缺乏SRF的小鼠表现出动脉收缩能力受损和大动脉直径增加,这是大动脉病的特征.
- 尽管有动脉病特征,但缺乏Srf的小鼠受到AngII诱导的动脉病变的保护,这表明了适应机制.
结论:
- 在维持动脉收缩性和调节年龄相关的转录变化方面,SRF起着至关重要的作用.
- 通过YAP/TAZ和Lats2通道,SRF的耗尽会诱导大关节病变,但会通过YAP/TAZ和Lats2通道保护高血压诱导的动脉瘤.
- 了解SRF的作用,可以了解与年龄有关的大动脉功能障碍以及潜在的治疗点.
关键词:
ангиотензин II 的使用生物信息学是一种生物信息学.心血管疾病心血管疾病细胞骨架 细胞骨架基因淘汰赛 基因淘汰赛这种高血压,高血压.在法律上,它是Leiomodin.肌肉神经系统 (myocardin) 是一个肌酸氨酸轻链激酶的作用平滑肌肉的 γ-actin 的作用.更多相关视频
09:32Measurement of Pulse Propagation Velocity, Distensibility and Strain in an Abdominal Aortic Aneurysm Mouse Model
Published on: February 23, 2020
6.1K
08:41Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
9.7K
相关概念视频
Aging
34
Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
34
Inflammation
52.1K
Overview
52.1K
