Z Kardiol 94: Suppl 2 (2005)

Hämatopoetische Stammzellen in der Atherosklerose

R. Braun-Dullaeus1

1Med. Klinik und Poliklinik II/Kardiologie, Technische Universität Dresden, Herzzentrum Dresden Universitätsklinik, Dresden, BusinessLogic.Land;

Recently we have appreciated that inflammatory mechanisms couple dyslipidemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. In addition to inflammation, a key process of atherosclerosis involves accumulation and proliferation of vascular smooth muscle cells (SMCs) within the intima. The origin of SMCs in the atherosclerotic plaque is intriguing. The prevailing theory of smooth muscle cell contribution to vessel lesion is that in pathological states, such as injury and atherosclerosis, SMCs migrate to the intima from the media of the vessel. This theory, which has persisted for three decades, is now being challenged by results from models of hyperlipidemia-induced atherosclerosis, post-angioplasty restenosis, transplant arteriosclerosis, and human allograft studies indicating that a portion of the cells bearing SMC differentiation markers in intimal lesions may have originated from the hematopoietic system and/or circulating progenitor cells. Furthermore, cells with the capacity to differentiate into SMC have been found in human blood. This review highlights the recent findings on circulating vascular precursors and describes the potential of therapeutic strategies for vascular diseases through targeting their mobilization, homing, differentiation and proliferation.

http://www.abstractserver.de/dgk2005/ht/abstracts/H266.htm