Insight...blocking the interaction between CD40L and Mac1, an interaction that was previously described to be crucial in atherosclerosis, does not affect restenosis: CD40-CD40L: A Janus-faced interaction

摘要

An extensive body of experimental and clinical evidence implicates inflammation with neointimal hyperplasia and restenosis after coronary interventions (1,2). Following injury to the vessel wall a network of inflammatory cellular and molecular regulatory pathways are activated. Vascular inflammation involves complex heterotypic interactions between endothelial cells, platelets, and inflammatory cells including neutrophils, monocytes, lymphocytes, and mast cells. Under normal circumstances, the cellular and molecular processes governing these responses mediate repair and vascular healing. In pathological conditions, however, dys-regulation of inflammatory responses results in persistent inflammation and adverse arterial remodeling contributing to the development of clinical complications such as restenosis.