Antibody-mediated endothelial cell damage via nitric oxide

Y. S. Lin, C. F. Lin, H. Y. Lei, H. S. Liu, T. M. Yeh, S. H. Chen, C. C. Liu

研究成果: Review article同行評審

47 引文 斯高帕斯(Scopus)


Vascular disorders, resulting from endothelial cell dysfunction, may be caused by various stimuli, including infectious, pathogens, cytotoxic reagents, and pathophysiological mechanisms mediated by immune responses. Endothelial cell dysfunction characterized by apoptosis and abnormal immune activation is, at least in part, induced by anti-endothelial cell antibody (AECA) in some cases of autoimmune disease. However, the molecular mechanisms of AECA-mediated pathogenetic damage to host vascular system remain unclear. The dual role of nitric oxide (NO) both in endothelial cell apoptosis and survival has been described. In this paper, endothelial cell apoptosis caused by the presence of cross-reactive AECA via a NO-mediated mechanism is demonstrated in dengue virus infection. Endothelial cells undergo apoptosis via the mitochondria-dependent pathway that is regulated by NO production. NO-regulated endothelial cell injury thus may play a role in the disruption of vessel endothelium and contribute to the AECA-induced pathogenesis of vasculopathy. The modulation of NO may provide the therapeutic strategies for autoimmune diseases by preventing the AECA-mediated endothelial cell damage.

頁(從 - 到)213-221
期刊Current Pharmaceutical Design
出版狀態Published - 2004

All Science Journal Classification (ASJC) codes

  • 藥理
  • 藥物發現


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