Soehnlein Oliver, Weber Christian
Institute for Molecular Cardiovascular Research, RWTH University Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.
Semin Immunopathol. 2009 Jun;31(1):35-47. doi: 10.1007/s00281-009-0141-z. Epub 2009 Feb 24.
Chronic inflammation is the underlying pathophysiological mechanism of atherosclerosis. Prominent suspects being involved in atherosclerosis are lymphocytes, platelets, and endothelial cells. However, recent advances suggest a potent role for myeloid leukocytes, specifically monocyte subsets, polymorphonuclear leukocytes, and mast cells. These three cell types are not just rapidly recruited or already reside in the vascular wall but also initiate and perpetuate core mechanisms in plaque formation and destabilization. Dendritic cell subsets as well as endothelial and smooth muscle progenitor cells may further emerge as important regulators of atheroprogression. To stimulate further investigations about the contribution of these myeloid cells, we highlight the current mechanistic understanding by which these cells tune atherosclerosis.
慢性炎症是动脉粥样硬化潜在的病理生理机制。参与动脉粥样硬化的主要可疑因素是淋巴细胞、血小板和内皮细胞。然而,最近的研究进展表明髓系白细胞,特别是单核细胞亚群、多形核白细胞和肥大细胞发挥着重要作用。这三种细胞类型不仅能迅速募集或早已存在于血管壁中,还能启动并维持斑块形成和不稳定的核心机制。树突状细胞亚群以及内皮和平滑肌祖细胞可能会进一步成为动脉粥样硬化进展的重要调节因子。为了推动对这些髓系细胞作用的进一步研究,我们着重介绍目前对这些细胞调节动脉粥样硬化机制的理解。