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交感性超内内驱动腹腔大动脉动脉瘤的发展,通过促进血管光滑肌细胞表型切换促进腹腔大动脉动脉瘤的发展

Zhenquan Tang¹, Jingfang Xie², Ming Jin¹

¹Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, China; Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, 510515 Guangzhou, China.

Journal of advanced research

|May 31, 2024

概括

交感性超内内转化通过改变血管光滑肌细胞 (VSMC) 现型,促进腹腔大动脉动脉瘤 (AAA) 的发展. 抑制这种神经生长可能为AAA提供一种新的治疗方法.

科学领域:

心血管生物学心血管生物学
血管生物学血管生物学
神经科学是一个神经科学.

背景情况:

交感性超内内化影响血管光滑肌细胞 (VSMC) 表型和血管疾病.
它在腹腔大动脉动脉瘤 (AAA) 发病过程中的特定作用仍然在很大程度上未被探索.

研究的目的:

阐明同情性超内核在促进AAA发展中的作用.
确定参与这个过程的潜在分子机制.

主要方法:

使用西式涂抹和免疫化学染色来评估交感性超内内.
在有或没有交感性无神经的小鼠模型中研究了AAA的发展 (性瘤切除术或6-OHDA的使用).
通过转录组分析,功能研究和Sema4D淘汰小鼠来研究机制.

主要成果:

在AAA小鼠模型和人类AAA患者中观察到交感超内置.
消除交感性超内内转显著降低了AAA的发展和进展.
交感性超内内转化通过细胞外ATP (eATP) -P2rx4-p38信号传递促进VSMC的表型切换.
骨质细胞衍生的Sema4D通过结合Plxnb1来诱导交感性超内核,在缺乏AAA的小鼠中改善AAA.

结论:

由Sema4D驱动的交感性超内内转,通过通过eATP/P2rx4/p38通路促进VSMC表型切换来加速AAA进展.
准交感性超内内向是AAA的一种潜在的治疗策略.

关键词:

腹腔大动脉动脉瘤腹腔大动脉动脉瘤骨质细胞类似的细胞.这就是Sema4D的意义.交感性超内内转化 (Sympathetic hyperinnervation) 是一种超内转化.在VSMC中,VSMC是VSMC.

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