Deparment of Pathology and Laboratory Medicine, University of British Columbia, McDonald Research Laboratory, Room 292, St. Paul's Hospital, 1081 Burrard St., Vancouver, BC, V6Z 1Y6, Canada.
Trends Cardiovasc Med. 1998 Jan;8(1):19-24. doi: 10.1016/S1050-1738(97)00126-6.
Tumor necrosis factor (TNF) is a multifunctional cytokine that elicits various responses in endothelial cells that can be summarized as being proinflammatory and procoagulant. Apoptosis refers to a genetically programmed form of cell death in which the cell participates in its own demise. Although TNF can activate the death pathway in normal human endothelial cells, apoptosis only results when protein synthesis is blocked. This finding indicates that TNF elicits both survival and death pathways. Endothelial cell apoptosis has been reported in various pathophysiologic situations from vascular development to immune disorders and atherosclerosis. The role of TNF-mediated endothelial death in these situations remains to be defined.
肿瘤坏死因子（TNF）是一种多功能细胞因子，可在血管内皮细胞中引发各种反应，这些反应可概括为促炎和促凝。细胞凋亡是指一种基因编程的细胞死亡形式，其中细胞参与自身的死亡。虽然 TNF 可以激活正常人类内皮细胞的死亡途径，但只有在蛋白质合成受阻时才会导致细胞凋亡。这一发现表明，TNF 可引发生存和死亡途径。在从血管发育到免疫紊乱和动脉粥样硬化等各种病理生理情况下，已经报道了内皮细胞凋亡。在这些情况下，TNF 介导的内皮细胞死亡的作用仍有待确定。
