Inflammasome and cardiovascular diseases

被引:7
作者
Connat, J. -L. [1 ]
机构
[1] Univ Bourgogne, Fac Med, IFR Sante STIC 100, Lab Physiopathol & Pharmacol Cardiovasc Expt, F-21000 Dijon, France
来源
ANNALES DE CARDIOLOGIE ET D ANGEIOLOGIE | 2011年 / 60卷 / 01期
关键词
Inflammasome; NOD-like receptor; NLR; NALP; NLR mutations; Atherosclerosis; Oxydative stress; KAPPA-B ACTIVATION; NALP3; INFLAMMASOME; INTERLEUKIN-1-BETA; NOD2; ATHEROSCLEROSIS; INFECTION; CASPASE-1; SUSCEPTIBILITY; PROTEIN; GENE;
D O I
10.1016/j.ancard.2010.07.011
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
NOD-like receptors (NLRs) constitute a recently identified family of intracellular pattern recognition receptors which contains more than 20 members in mammals. Some of the NLRs, the NALP subfamily, constituted from 14 members, many of them without actual identified role, form multiproteic complex known as inflammasome, that initiate inflammation by processing inactive pro-caspase-1 to its active form, allowing the cleavage and subsequent activation of pro-IL-1 beta and pro-IL-18. We review the identified roles of NLRs in pathologies and argue for the role of inflammasome in the development of cardiovascular diseases. The atherogenic cytokines IL-1 beta and IL-18 are matured in NLRPs inflammasomes. Immunocytochemistry shows that Nlrp3 inflammasome is expressed in plaques, upregulated and activated in the CD11b(+)Gr1(high) atherosclerosis-prone monocyte subset and modulated by oxLDL in murine macrophages. These results provide an unexpected role for Nlrp3 inflammasome in atherosclerosis. (C) 2010 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:48 / 54
页数:7
相关论文
共 61 条
  • [1] NALP3 forms an IL-lβ-Processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder
    Agostini, L
    Martinon, F
    Burns, K
    McDermott, MF
    Hawkins, PN
    Tschopp, J
    [J]. IMMUNITY, 2004, 20 (03) : 319 - 325
  • [2] Membrane recruitment of NOD2 in intestinal epithelial cells is essential for nuclear factor-κB activation in muramyl dipeptide recognition
    Barnich, N
    Aguirre, JE
    Reinecker, HC
    Xavier, R
    Podolsky, DK
    [J]. JOURNAL OF CELL BIOLOGY, 2005, 170 (01) : 21 - 26
  • [3] BERNARDINI C, 2009, CELL STRESS CHAPERON
  • [4] BILLIET L, 2009, THIOREDOXINE 1 NOUVE
  • [5] BLACK RA, 1989, J BIOL CHEM, V264, P5323
  • [6] Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin
    Boyden, ED
    Dietrich, WF
    [J]. NATURE GENETICS, 2006, 38 (02) : 240 - 244
  • [7] Selective NOD1 agonists cause shock and organ injury/dysfunction in vivo
    Cartwright, Neil
    Murch, Oliver
    McMaster, Shaun K.
    Paul-Clark, Mark J.
    van Heel, David A.
    Ryffel, Bernhard
    Quesniaux, Valerie F. J.
    Evans, Timothy W.
    Thiemermann, Christoph
    Mitchell, Jane A.
    [J]. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2007, 175 (06) : 595 - 603
  • [8] The Nalp3 inflammasome is essential for the development of silicosis
    Cassel, Suzanne L.
    Eisenbarth, Stephanie C.
    Iyer, Shankar S.
    Sadler, Jeffrey J.
    Colegio, Oscar R.
    Tephly, Linda A.
    Carter, A. Brent
    Rothman, Paul B.
    Flavell, Richard A.
    Sutterwala, Fayyaz S.
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (26) : 9035 - 9040
  • [9] MOLECULAR-CLONING OF THE INTERLEUKIN-1-BETA CONVERTING ENZYME
    CERRETTI, DP
    KOZLOSKY, CJ
    MOSLEY, B
    NELSON, N
    VANNESS, K
    GREENSTREET, TA
    MARCH, CJ
    KRONHEIM, SR
    DRUCK, T
    CANNIZZARO, LA
    HUEBNER, K
    BLACK, RA
    [J]. SCIENCE, 1992, 256 (5053) : 97 - 100
  • [10] Interleukin-1β, interleukin-18, and the interleukin-1β converting enzyme
    Dinarello, CA
    [J]. MOLECULAR MECHANISMS OF FEVER, 1998, 856 : 1 - 11