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Acute and chronic inflammation is associated with changes in microvascular form and function. At rest, endothelial cells maintain a nonthrombogenic, nonreactive surface at the interface between blood and tissue. However, on activation by proinflammatory mediators, the endothelium becomes a major participant in the generation of the inflammatory response. These functions of endothelium are modified by the other cell populations of the microvessel wall, namely pericytes, and smooth muscle cells. This article reviews recent advances in understanding the roles played by microvessels in inflammation.
Pober et al. (Thu,) studied this question.
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