Leukocyte Behavior in Atherosclerosis, Myocardial Infarction, and Heart Failure

American Association for the Advancement of Science (AAAS) - Tập 339 Số 6116 - Trang 161-166 - 2013
Filip K. Świrski1, Matthias Nahrendorf1
1Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA

Tóm tắt

Cardiovascular diseases claim more lives worldwide than any other. Etiologically, the dominant trajectory involves atherosclerosis, a chronic inflammatory process of lipid-rich lesion growth in the vascular wall that can cause life-threatening myocardial infarction (MI). Those who survive MI can develop congestive heart failure, a chronic condition of inadequate pump activity that is frequently fatal. Leukocytes (white blood cells) are important participants at the various stages of cardiovascular disease progression and complication. This Review will discuss leukocyte function in atherosclerosis, MI, and heart failure.

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Tài liệu tham khảo

10.1056/NEJMra1112570

D. E. Bloom et al . The Global Economic Burden of Noncommunicable Diseases (World Economic Forum Geneva 2011).

10.1161/CIRCULATIONAHA.106.676890

H. C. Stary Atlas of Atherosclerosis: Progression and Regression (Parthenon New York 1999).

10.1038/nri1882

Gerrity R. G., The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes into foam cells in fatty lesions. Am. J. Pathol. 103, 181 (1981).72349617234961

Gerrity R. G., The role of the monocyte in atherogenesis: II. Migration of foam cells from atherosclerotic lesions. Am. J. Pathol. 103, 191 (1981).72349627234962

10.1016/j.cell.2011.04.005

10.1038/nature08938

10.1371/journal.pone.0011765

10.1161/ATVBAHA.108.176644

10.1038/cddis.2011.18

10.1016/j.cell.2012.06.054

10.1126/science.1178331

10.1172/JCI29950

10.1172/JCI28549

10.1161/CIRCULATIONAHA.111.061986

10.1126/science.1189731

10.1172/JCI57559

10.1016/j.stem.2012.04.024

10.1007/s11883-012-0274-8

10.1161/CIRCULATIONAHA.107.745091

10.1161/CIRCULATIONAHA.107.743872

10.1038/ni.2205

10.1172/JCI38911

10.1172/JCI43802

10.1016/j.cmet.2012.01.022

10.1084/jem.20070885

10.1084/jem.20090866

10.1084/jem.20082129

10.1016/j.immuni.2011.09.014

10.1172/JCI61758

10.1084/jem.20080752

10.1016/j.clim.2009.07.002

10.1038/nrcardio.2011.62

10.1097/MOL.0b013e32834adaf3

10.1016/j.tcm.2012.06.011

10.1073/pnas.92.9.3893

10.1161/01.ATV.14.1.32

10.1161/CIRCULATIONAHA.110.961714

10.1038/nm1601

10.1038/nm810

10.1371/journal.pone.0036814

10.1161/01.RES.0000163017.13772.3a

10.1016/j.jacc.2011.08.066

10.1161/CIRCULATIONAHA.111.044164

10.1161/CIRCULATIONAHA.111.052126

10.1084/jem.20111009

10.1016/j.jacc.2009.08.089

10.1038/nbt.1989

10.1126/science.1175202

10.1038/nature11260

10.1016/j.atherosclerosis.2010.06.022

10.1126/science.1230721

10.1038/nature10992

10.1161/CIRCHEARTFAILURE.108.827071

10.1016/j.jacc.2009.04.021

10.1093/eurheartj/ehr388

10.1182/blood-2004-05-1831

10.1126/science.1230720