Matrix metalloproteinases in cardiovascular diseaseRôle des métalloprotéinases matricielles dans la maladie cardiovasculaire

https://doi.org/10.1016/S0828-282X(06)70983-7Get rights and content

Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that are regulated by inflammatory signals to mediate changes in extracellular matrix. Members of the MMP family share sequence homology, act on interstitial protein substrates, acutely participate in inflammatory processes and chronically mediate tissue remodelling. MMPs are important in vascular remodelling, not only in the overall vasculature architecture but also, more importantly, in the advancing atherosclerotic plaque. MMP activation modifies the architecture of the plaque and may directly participate in the process of plaque rupture. MMPs also participate in cardiac remodelling following myocardial infarction and development of dilated cardiomyopathy. Soluble MMPs are now potential biomarkers in delineating cardiovascular risk for plaque rupture and coronary risk. They also constitute innovative direct or indirect targets to modify cardiovascular tissue remodelling in atherosclerosis and heart failure.

Les métalloprotéinases matricielles (MPM) forment une famille d’enzymes protéolytiques dont la régulation est assurée par des signaux inflammatoires qui amènent des changements au niveau de la matrice extracellulaire. Les membres de la famille des MPM partagent une homologie séquentielle, agissent sur les substrats des protéines interstitielles, participent intensément aux processus inflammatoires et influent à plus long terme sur le remodelage tissulaire. Les MPM sont importantes dans le remodelage des vaisseaux, car elles affectent non seulement leur architecture globale, mais également et surtout, la progression de la plaque d’athérome. L’activation des MPM modifie l’architecture de la plaque et peut participer directement à sa rupture. Les MPM sont en outre impliquées dans le remodelage cardiaque après un infarctus du myocarde et dans le développement de la myocardiopathie dilatée. Les MPM solubles sont désormais des biomarqueurs potentiels qui permettent d’identifier le risque cardiovasculaire associé à la rupture de la plaque et le risque coronarien. Elles constituent en outre de nouvelles cibles directes ou indirectes pour modifier le remodelage du tissu cardiovasculaire en présence d’athérosclérose et d’insuffisance cardiaque.

References (25)

  • J.A. Stewart et al.

    Cardiac mast cell- and chymase-mediated matrix metalloproteinase activity and left ventricular remodeling in mitral regurgitation in the dog

    J Mol Cell Cardiol

    (2003)
  • J. Orbe et al.

    Different expression of MMPs/TIMP-1 in human atherosclerotic lesions. Relation to plaque features and vascular bed

    Atherosclerosis

    (2003)
  • J.F. Woessner

    Matrix metalloproteinases and their inhibitors in connective tissue remodeling

    FASEB J

    (1991)
  • I. Massova et al.

    Matrix metalloproteinases: Structures, evolution, and diversification

    FASEB J

    (1998)
  • F.G. Spinale et al.

    A matrix metalloproteinase induction/activation system exists in the human left ventricular myocardium and is upregulated in heart failure

    Circulation

    (2000)
  • S. Heymans et al.

    Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure

    Nat Med

    (1999)
  • M. Sun et al.

    Excessive tumor necrosis factor activation after infarction contributes to susceptibility of myocardial rupture and left ventricular dysfunction

    Circulation

    (2004)
  • W. Wang et al.

    Intracellular action of matrix metalloproteinase-2 accounts for acute myocardial ischemia and reperfusion injury

    Circulation

    (2002)
  • J.B. Knox et al.

    Evidence for altered balance between matrix metalloproteinases and their inhibitors in human aortic diseases

    Circulation

    (1997)
  • Z.S. Galis et al.

    Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques

    J Clin Invest

    (1994)
  • A. Luttun et al.

    Loss of matrix metalloproteinase-9 or matrix metalloproteinase-12 protects apolipoprotein E-deficient mice against atherosclerotic media destruction but differentially affects plaque growth

    Circulation

    (2004)
  • J.K. Lee et al.

    A serine elastase inhibitor reduces inflammation and fibrosis and preserves cardiac function after experimentally-induced murine myocarditis

    Nat Med

    (1998)
  • Cited by (148)

    • Protease detection in the biosensor era: A review

      2024, Biosensors and Bioelectronics
    View all citing articles on Scopus
    View full text