Vascular Endothelial Cell Dysfunction in Preeclampsia

Abstract

In the early 1980s, physicians and scientists began to gain an appreciation of the physiological importance of the endothelium, the simple unicellular layer lining the luminal surface of blood vessels. Indeed, in Chesley’s first, single-authored edition of this text, the reference to this term was confined to the “endotheliosis” lesion of the renal glomerulus. We now recognize that endothelial cells are critical sensors of the milieu interieur and potent regulators of vascular tone, organ perfusion, and ischemia. The “endothelial hypothesis” of preeclampsia etiology provides for a convergence of several factors thought to play fundamental roles in its pathogenesis: leukocytes, platelets, cytokines, fatty acids, oxygen free radicals, placental microvesicles, cell-free DNA fragments, “antiangiogenic” factors, and autoantibodies are all considered.