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S100A4 是胸前大动脉解剖的一个关键促进者

Jiajun Shi¹, Wenjun Yu^1,2,3, Chuan Liang^1,2,3

¹Department of Cardiovascular Surgery, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.

International journal of biological sciences

|January 2, 2024

概括

细胞外S100A4通过破坏细胞外矩阵恒温来加剧胸前大动脉解剖 (TAD). 抑制S100A4可能为TAD预防和治疗提供一个新的治疗点.

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.
血管生物学血管生物学

背景情况:

胸前动脉解剖 (TAD) 是一种严重的心血管疾病,死亡率高.
血管光滑肌细胞 (VSMCs) 在TAD病变发生过程中至关重要.
细胞外S100A4在VSMC和TAD中的确切作用和机制尚不清楚.

研究的目的:

调查S100A4在VSMC调控和TAD中的作用.
阐明关联S100A4与TAD进展的潜在分子机制.

主要方法:

转录组数据分析以确定大动脉剖析中的枢纽基因.
用S100A4过度表达和淘汰小鼠进行TAD的小鼠模型.
评估VSMC表型过渡和细胞外矩阵 (ECM) 稳态.

主要成果:

S100A4被确定为大动脉剖析中的关键枢纽基因.
S100A4过度表达使TAD恶化,而敲击改善了它.
S100A4与lysyl氧化酶 (LOX) 相互作用,减少成熟的LOX和弹性纤维沉积,破坏ECM平衡.

结论:

S100A4通过与LOX相互作用促进TAD,从而减少弹性纤维沉积和ECM破坏.
S100A4诱导成熟LOX的溶酶体降解.
S100A4代表了胸前大动脉剖析的潜在治疗标.

关键词:

细胞外矩阵是细胞外矩阵.Lysyl 氧化酶是一种溶解氧化剂.在 S100A4 中使用.胸前大动脉剖析胸前大动脉剖析血管光滑肌细胞是血管光滑肌细胞.

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