The Molecular Mechanism Underlying Atherosclerotic Plaque Rupture : Impact on Cysteinyl Cathepsin and Vascular Smooth Muscle Cell Apoptosis

尽管最近的研究表明，半胱氨酸组织蛋白酶（半胱氨酸组织蛋白酶）参与细胞凋亡，但其在动脉粥样硬化斑块破坏中的确切机制尚不清楚。在这里，我们重点研究猫在斑块破裂中的作用，使用小鼠颈动脉斑块破裂模型。我们已经观察到，CatS涉及血管平滑肌细胞凋亡，并有助于斑块破裂。CatS是动脉粥样硬化斑块组成和破坏的重要决定因素，使CatS成为药物预防动脉粥样硬化斑块易损的一个有吸引力的靶点。

Although recent studies have suggested that cysteinyl cathepsins(Cats) participate in cell apoptosis, the Cat-related precise mechanism of in atherosclerotic plaque disruption remains poorly understood. Here, we focused to investigate the role of Cat in plaque rupture using a mouse carotid artery plaque rupture model. We have observed that CatS involves vascular smooth muscle cell apoptosis and contributes to plaque rupture. CatS is an important determination of atherosclerotic plaque composition and disruption, rendering CatS an attractive target for pharmaceutical prevention in atherosclerotic plaque vulnerability.