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由ATOX1驱动的ECM降解和血管光滑肌细胞亡加速了大动脉剖析进展

Yuling Xie¹, Xinfan Lin¹, Xu Han²

¹Department of Cardiovascular Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China; Key Laboratory of Cardio-Thoracic Surgery (Fujian Medical University), Fujian Province University, Fuzhou, Fujian, China; Fujian Provincial Center for Cardiovascular Medicine, Fuzhou, Fujian, China.

Biochimica et biophysica acta. Molecular basis of disease

|December 18, 2025

概括

抗氧化剂-1 (ATOX1) 蛋白在大动脉剖析 (AD) 中升高. 抑制ATOX1减少了细胞外基质降解和细胞亡,为AD提供了潜在的新治疗策略.

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.
生物化学生化学

背景情况:

大动脉剖析 (AD) 涉及细胞外基质 (ECM) 降解和血管光滑肌细胞 (VSMC) 亡.
抗氧化剂-1 (ATOX1) 在AD病变发生中的作用,特别是ECM降解和VSMC亡,需要进一步研究.

研究的目的:

阐明ATOX1在阿尔茨海默病发展中的作用.
研究ATOX1作为阿尔茨海默病的潜在治疗点.

主要方法:

高通量测序确定了AD患者ATOX1表达的增加.
使用组织染色,RT-PCR和西部斑点的验证证实了AD模型和细胞中ATOX1的升高.
在体外研究涉及人类大动脉血管光滑肌细胞 (HAVSMCs) 中的ATOX1沉默和药理抑制 (DC_AC50).
在体内研究中,在a-aminopropionitrile (BAPN) 诱导的小鼠模型中,利用腺相关病毒载体9 (AAV9) 进行向性淘汰和药理学抑制.
研究了miR-133b和ATOX1.1.之间的监管关系.

主要成果:

在AD患者,小鼠模型和 ангиотензинII诱导的HAVSMC中,ATOX1的表达显著增加.
沉默或抑制ATOX1降低了HAVSMC中的铜离子水平,矩阵金属蛋白酶 (MMP) 分泌和亡.
在小鼠模型中,针对性地降低或药理上抑制ATOX1减缓了AD的进展.
miR-133b,在AD下调,与ATOX1相反相关,可以逆转ATOX1诱导的影响.
在小鼠中,miR-133b的过度表达减弱了AD的进展.

结论:

抑制ATOX1可能会减轻ECM降解和VSMC亡,从而减缓AD的进展.
抑制ATOX1是一种有前途的治疗策略,用于大动脉解剖.

关键词:

抗氧化剂-1是一种抗氧化剂.动脉剖析是一个大动脉剖析.大动脉血管平滑肌肉细胞细胞灭亡 (apoptosis) 是一种死亡的过程.矩阵金属蛋白酶是一种金属蛋白酶.微型RNA-133bbb是什么意思

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