Yao Bo-Chen, Meng Ling-Bing, Hao Meng-Lei, Zhang Yuan-Meng, Gong Tao, Guo Zhi-Gang
1 Graduate College, Tianjin Medical University, Tianjin, China.
2 Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, China.
J Int Med Res. 2019 Apr;47(4):1429-1440. doi: 10.1177/0300060519826820. Epub 2019 Feb 24.
Chronic stress refers to the non-specific systemic reaction that occurs when the body is stimulated by various internal and external negative factors over a long time. The physiological response to chronic stress exposure has long been recognized as a potent modulator in the occurrence of atherosclerosis. Furthermore, research has confirmed the correlation between atherosclerosis and cardiovascular events. Chronic stress is pervasive during negative life events and may lead to the formation of plaque. Several epidemiological studies have shown that chronic stress is an independent risk factor for the development of vascular disease and for increased morbidity and mortality in patients with pre-existing coronary artery disease. One possible mechanism for this process is that chronic stress causes endothelial injury, directly activating macrophages, promoting foam cell formation and generating the formation of atherosclerotic plaque. This mechanism involves numerous variables, including inflammation, signal pathways, lipid metabolism and endothelial function. The mechanism of chronic stress in atherosclerosis should be further investigated to provide a theoretical basis for efforts to eliminate the effect of chronic stress on the cardiocerebral vascular system.
慢性应激是指机体在长期受到各种内外源性负面因素刺激时所产生的非特异性全身反应。长期以来,人们一直认为对慢性应激暴露的生理反应是动脉粥样硬化发生过程中的一个重要调节因素。此外,研究已经证实动脉粥样硬化与心血管事件之间存在关联。在负面生活事件中,慢性应激普遍存在,可能导致斑块形成。多项流行病学研究表明,慢性应激是血管疾病发生发展以及已有冠状动脉疾病患者发病率和死亡率增加的独立危险因素。这一过程的一种可能机制是,慢性应激导致内皮损伤,直接激活巨噬细胞,促进泡沫细胞形成并引发动脉粥样硬化斑块的形成。该机制涉及众多变量,包括炎症、信号通路、脂质代谢和内皮功能。应进一步研究慢性应激在动脉粥样硬化中的作用机制,为消除慢性应激对心脑血管系统影响的努力提供理论依据。