Thorin-Trescases Nathalie, Voghel Guillaume, Farhat Nada, Drouin Annick, Gendron Marie-Ève, Thorin Eric
Université de Montréal,Département de chirurgie, Institut de cardiologie de Montréal, centre de recherche, 5000, rue Bélanger est, Montréal (Québec) H1T 1C8 Canada.
Med Sci (Paris). 2010 Oct;26(10):875-80. doi: 10.1051/medsci/20102610875.
In order to maintain cellular homeostasis against endogenous and exogenous aggressions, different cellular mechanisms of defence, maintenance and repair are continuously activated throughout life. Hormesis, a concept based on the fact that mild stresses protect cells against subsequent stresses, amplifies the efficacy of the cellular mechanisms of defence and repair. Ageing, senescence and ultimately death, result from the exhaustion of these mechanisms maintaining cellular functions. One of the major sources of vascular endothelial damage is oxidative stress. The age-dependent shift in the redox environment towards pro-oxidation contributes to a progressive compensatory remodelling of the endothelium, an accumulation of damages, and its dysfunction, the premises for atherosclerosis. We propose that in agreement with the concept of hormesis, a moderate exposure during endothelial maturation to mild physiological oxidative stressors determines -vascular longevity.
为了维持细胞内环境稳定以抵御内源性和外源性侵害，一生中不同的细胞防御、维持和修复机制会持续被激活。应激适应是基于轻度应激可保护细胞免受后续应激这一事实的概念，它增强了细胞防御和修复机制的功效。衰老、细胞衰老以及最终的死亡，是由维持细胞功能的这些机制耗竭所致。血管内皮损伤的主要来源之一是氧化应激。氧化还原环境随年龄向促氧化方向的转变，促成了内皮的渐进性代偿性重塑、损伤积累及其功能障碍，而这些正是动脉粥样硬化的前提条件。我们提出，与应激适应概念一致，在内皮成熟过程中适度暴露于轻度生理性氧化应激源可决定血管寿命。
