Endothelial cell dysfunction, injury and death.
Vascular endothelial cells (ECs) perform a number of functions required to maintain homeostasis. Inflammation can cause EC injury and death which disrupt these processes and result in endothelial dysfunction. Three common mediators of EC injury in inflammation are macrophage-derived cytokines, such as tumour necrosis factor (TNF); neutrophil-generated reactive oxygen species (ROS) and cytolytic T lymphocytes (CTL). Here we describe the distinct but overlapping biochemical pathways of injury elicited by these different agents.
Pober
J S
JS
The Boyer Center for Molecular Medicine, Yale University School of Medicine, 295 Congress Avenue, Room 454, New Haven, CT 06510, USA. Jordan.pober@yale.edu
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D000818:Animals; D017209:Apoptosis; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D053804:Granzymes / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology; D008264:Macrophages / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D013602:T-Lymphocytes, Cytotoxic / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D053804:Granzymes