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系统识别和功能验证CASP10作为在动脉样硬化中的内皮质炎的DNA损伤反应驱动器

Xiangrong Meng¹, Kejian Zhang², Yu Xi¹

¹Department of Laboratory Diagnosis, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.

Journal of cellular and molecular medicine

|February 17, 2026

概括

DNA损伤反应 (DDR) 基因CASP10是识别不稳定的动脉样硬化斑块的关键生物标志物. 向CASP10可能会减少内皮细胞死亡并稳定斑块.

科学领域:

心血管生物学心血管生物学
分子病理学分子病理学
炎症研究炎症研究

背景情况:

动脉样硬化 (AS) 是一种慢性炎症性疾病,其特征是内皮功能障碍和斑块不稳定.
在内皮细胞命运中的DNA损伤反应 (DDR) 的作用及其在AS病变发生中的具体参与尚未完全理解.

研究的目的:

为了确定与DDR相关的生物标志物用于AS.
为了研究在动脉样硬化病变内的内皮质皮质灭亡中DDR的机制.

主要方法:

对66个与DDR相关的基因进行分析,以便在区分AS病变阶段和斑块稳定性方面的诊断准确性.
单细胞RNA测序以评估CASP10在内皮细胞中的表达.
在体外功能实验中使用HUVECs来确定CASP10在ox-LDL诱导的DNA损伤和热的作用.

主要成果:

一个由66个DDR基因组成的小组准确地区分了早期和晚期AS病变以及稳定和不稳定的斑块.
CASP10被确定为AS斑块不稳定的顶级诊断生物标志物 (AUC=0.991),并且在AS斑块的内皮细胞上调.
发现CASP10对于调解ox-LDL诱导的DNA损伤和灭,涉及γH2AX,NLRP3,GSDMD-N和IL-1β,是必不可少和足够的.

结论:

CASP10是一种可靠的生物标志物,用于识别不稳定的动脉样硬化斑块.
在AS中,CASP10充当了DNA损伤和内皮皮质亡之间的关键环节.
向CASP10为稳定动脉样硬化斑块和减少内皮细胞死亡提供了潜在的治疗策略.

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