Circulation Research. 2001;88:877-887
doi: 10.1161/hh0901.090440
doi: 10.1161/hh0901.090440
© 2001 American Heart Association, Inc.
Review |
Anti-Inflammatory Mechanisms in the Vascular Wall
From The Institut National de la Santé et de la Recherche Médicale, INSERM U541 and Institut Fédératif de Recherche "Circulation-Paris 7," Hôpital Lariboisière, Paris, France.
Correspondence to Alain Tedgui, PhD, INSERM U541, 41, Bd de la Chapelle, 75475 Paris, Cedex 10, France. E-mail tedgui{at}infobiogen.fr
Abstract—The
role of vascular cells during inflammation is critical and is of
particular importance in inflammatory diseases, including
atherosclerosis, ischemia/reperfusion, and
septic shock. Research in vascular biology has progressed remarkably in
the last decade, resulting in a better understanding of the vascular
cell responses to inflammatory stimuli. Most of the vascular
inflammatory responses are mediated through the I
B/nuclear
factor-B system. Much recent work shows that vascular inflammation
can be limited by anti-inflammatory counteregulatory mechanisms that
maintain the integrity and homeostasis of the vascular wall. The
anti-inflammatory mechanisms in the vascular wall involve
anti-inflammatory external signals and intracellular mediators. The
anti-inflammatory external signals include the anti-inflammatory
cytokines, transforming growth factor-ß, interleukin-10 and
interleukin-1 receptor antagonist, HDL, as well as some
angiogenic and growth factors. Physiological
laminar shear stress is of particular importance in protecting
endothelial cells against inflammatory activation. Its
effects are partly mediated through NO production. Finally,
endogenous cytoprotective genes or nuclear receptors, such
as the peroxisome proliferator–activated receptors, can be
expressed by vascular cells in response to proinflammatory stimuli to
limit the inflammatory process and the injury.
Key Words: endothelial cells • smooth muscle cells • inflammation • anti-inflammatory cytokines • shear stress
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