Involvement of CHOP in Arteriosclerosis Acceleration with Augmented Biological Stress Responses

动脉硬化过程受多种生物途径的相互作用影响，如炎症反应、氧化应激和内质网应激。众所周知，C/EBP同源蛋白（CHOP）在严重内质网应激下可诱导细胞凋亡，据报道其在斑块病变中表达上调。在CHOP-/-小鼠中，炎症因子和氧化应激标志物的表达受到抑制，可显著抑制袖带损伤诱导的新内膜形成和高胆固醇血症诱导的主动脉斑块形成。CHOP可能在增加潜在的病理性生物应激反应中发挥重要作用，并有助于血管重构和动脉粥样硬化的进展。

The processes of arteriosclerosis are affected by interactions among numerous biological pathways, such as responses to inflammation, oxidative stress and endoplasmic reticulum (ER)stress. C/EBP homologous protein (CHOP), which is well known to induce cellular apoptosis in response to severe ER stress, is reportedly up-regulated in plaque lesions. Cuff injury-induced neointimal formation and hypercholesterolemia-induced aortic plaque formation were markedly inhibited in CHOP-/-mice with suppressed aortic expressions of inflammatory factors and oxidative stress markers. CHOP may play important roles in augmenting potentially pathological biological stress responses and contribute to the progression of vascular remodeling and atherosclerosis.