Inflammatory mechanisms: The molecular basis of inflammation and disease

被引:403
作者
Libby, Peter [1 ,2 ]
机构
[1] Harvard Univ, Sch Med, Cambridge, MA 02138 USA
[2] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA
关键词
inflammation; cytokines; chronic disease; atherosclerosis; macrophages; arterial lesions; plaque rupture; thrombosis;
D O I
10.1301/nr.2007.dec.S140-S146
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Inflammation participates importantly in host defenses against infectious agents and injury, but it also contributes to the pathophysiology of many chronic diseases. Interactions of cells in the innate immune system, adaptive immune system, and inflammatory mediators orchestrate aspects of the acute and chronic inflammation that underlie diseases of many organs. A coordinated series of common effector mechanisms of inflammation contribute to tissue injury, oxidative stress, remodeling of the extracellular matrix, angiogenesis, and fibrosis in diverse target tissues. Atherosclerosis provides an example of a chronic disease that involves inflammatory mechanisms. Recruitment of blood leukocytes characterizes the initiation of this disease. Its progression involves many inflammatory mediators, modulated by cells of both innate and adaptive immunity. The complications of established atheroma, including plaque disruption and thrombosis, also intimately involve inflammation. Mastery of the inflammatory response should aid the development of novel strategies to predict disease susceptibility, target and monitor therapies, and ultimately develop new approaches to the prevention and treatment of chronic diseases associated with aging, such as atherosclerosis.
引用
收藏
页码:S140 / S146
页数:7
相关论文
共 55 条
[21]   INDUCIBLE INTERLEUKIN-1 GENE-EXPRESSION IN HUMAN VASCULAR SMOOTH-MUSCLE CELLS [J].
LIBBY, P ;
ORDOVAS, JM ;
BIRINYI, LK ;
AUGER, KR ;
DINARELLO, CA .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 78 (06) :1432-1438
[22]  
LIBBY P, 1986, AM J PATHOL, V124, P179
[23]   Inflammation and atherosclerosis [J].
Libby, P ;
Ridker, PM ;
Maseri, A .
CIRCULATION, 2002, 105 (09) :1135-1143
[24]  
Libby P, 2002, NATURE, V420, P868, DOI [10.1038/nature01323, 10.1161/ATVBAHA.108.179705]
[25]   MOLECULAR-BASES OF THE ACUTE CORONARY SYNDROMES [J].
LIBBY, P .
CIRCULATION, 1995, 91 (11) :2844-2850
[26]   Pathophysiology of coronary artery disease [J].
Libby, P ;
Theroux, P .
CIRCULATION, 2005, 111 (25) :3481-3488
[27]   EFFECTS OF FIBROUS CAP THICKNESS ON PEAK CIRCUMFERENTIAL STRESS IN MODEL ATHEROSCLEROTIC VESSELS [J].
LOREE, HM ;
KAMM, RD ;
STRINGFELLOW, RG ;
LEE, RT .
CIRCULATION RESEARCH, 1992, 71 (04) :850-858
[28]   Both early and delayed anti-CD40L antibody treatment induces a stable plaque phenotype [J].
Lutgens, E ;
Cleutjens, KBJM ;
Heeneman, S ;
Koteliansky, VE ;
Burkly, LC ;
Daemen, MJAP .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (13) :7464-7469
[29]   Reduction of atherosclerosis in mice by inhibition of CD40 signalling [J].
Mach, F ;
Schönbeck, U ;
Sukhova, GK ;
Atkinson, E ;
Libby, P .
NATURE, 1998, 394 (6689) :200-203
[30]  
Mach F, 1997, CIRCULATION, V96, P396