Endothelial Cell Dysfunction and Oxidative Stress

作者: Robert N. Taylor , Sandra T. Davidge , James M. Roberts

DOI: 10.1016/B978-0-12-374213-1.00009-4

关键词: Vascular endothelial growth factor BSelectinGrowth factorBiologyEndothelial stem cellEndothelial activationPreeclampsiaPathogenesisImmunologyPlatelet-derived growth factor receptor

摘要: Publisher Summary This chapter reviews findings relevant to endothelial cell biology in preeclampsia. Endothelial dysfunction preeclampsia results a variety of circulating factors, such as angiogenic metabolic and inflammatory mediators. activation or damage is manifest biochemically by the synthesis secretion products including prostanoids, endothelin-1 (ET-1), platelet-derived growth factor (PDGF), fibronectin, selectins, other molecules that influence vessel tone remodeling. When activated chronic pathological process, preeclampsia, these responses can create vicious cycle vasospasm, microthrombosis, disruption vascular integrity, serious physiologic disturbances which persist until inciting factor(s) eliminated. Evidence suggests pathogenesis involves plasma constituents induce and/or dysfunction. Given understanding epidemiology this disease, it highly probable placenta contributes factors responsible for In addition, considerable evidence maternal constitutional also are involved.

参考文章(283)
I Johnson, P Baker, J Brockelsby, R Hayman, A Ahmed, A Warren, VEGF via VEGF receptor-1 (Flt-1) mimics preeclamptic plasma in inhibiting uterine blood vessel relaxation in pregnancy: implications in the pathogenesis of preeclampsia. Laboratory Investigation. ,vol. 79, pp. 1101- 1111 ,(1999)
Bell Et, Renal Lesions in the Toxemias of Pregnancy. American Journal of Pathology. ,vol. 8, pp. 1- ,(1932)
Henning MORAWIETZ, Nicole DUERRSCHMIDT, Bernd NIEMANN, Jan GALLE, Tatsuya SAWAMURA, Juergen HOLTZ, Augmented endothelial uptake of oxidized low-density lipoprotein in response to endothelin-1. Clinical Science. ,vol. 103, ,(2002) , 10.1042/CS103S009S
S. T. Davidge, P. N. Baker, J. M. Roberts, NOS expression is increased in endothelial cells exposed to plasma from women with preeclampsia American Journal of Physiology-heart and Circulatory Physiology. ,vol. 269, ,(1995) , 10.1152/AJPHEART.1995.269.3.H1106
Satoshi Ogawa, Revati Shreeniwas, Caesar Butura, Jerold Brett, David M. Stern, Modulation of Endothelial Function by Hypoxia: Perturbation of Barrier and Anticoagulant Function, and Induction of a Novel Factor X Activator Advances in Experimental Medicine and Biology. ,vol. 281, pp. 303- 312 ,(1990) , 10.1007/978-1-4615-3806-6_32
Alain Kanfer, Jean-Frederic Bruch, Genevieve Nguyen, Ci Jiang He, Francoise Delarue, Antoine Flahault, C. Nessmann, Serge Uzan, Increased placental antifibrinolytic potential and fibrin deposits in pregnancy-induced hypertension and preeclampsia. Laboratory Investigation. ,vol. 74, pp. 253- 258 ,(1996)
Weiner Cp, Thrombotic microangiopathy in pregnancy and the postpartum period. Seminars in Hematology. ,vol. 24, pp. 119- 129 ,(1987)
A. Barden, D. Graham, L. J. Beilin, J. Ritchie, R. Baker, B. N. Walters, C. A. Michael, Neutrophil CD11B expression and neutrophil activation in pre-eclampsia. Clinical Science. ,vol. 92, pp. 37- 44 ,(1997) , 10.1042/CS0920037
I. Barroso, M. Gurnell, V. E. F. Crowley, M. Agostini, J. W. Schwabe, M. A. Soos, G. LI Maslen, T. D. M. Williams, H. Lewis, A. J. Schafer, V. K. K. Chatterjee, S. O'Rahilly, Dominant negative mutations in human PPARγ associated with severe insulin resistance, diabetes mellitus and hypertension Nature. ,vol. 402, pp. 880- 883 ,(1999) , 10.1038/47254
Leslie L. Waite, Amy K. Atwood, Robert N. Taylor, Preeclampsia, an implantation disorder. Reviews in Endocrine & Metabolic Disorders. ,vol. 3, pp. 151- 158 ,(2002) , 10.1023/A:1015411113468