High Blood Pressure & Cardiovascular Prevention

, Volume 17, Issue 4, pp 201–208

Matrix Metalloproteinases and their Inhibitors in Hypertensive Cardiac Remodelling


    • Department of Clinical MedicineUniversity of Insubria
  • Andrea M. Maresca
    • Department of Clinical MedicineUniversity of Insubria
    • Ospedale di Circolo
  • Anna M. Grandi
    • Department of Clinical MedicineUniversity of Insubria
    • Ospedale di Circolo
Review Article

DOI: 10.2165/11311960-000000000-00000

Cite this article as:
Marchesi, C., Maresca, A.M. & Grandi, A.M. High Blood Press Cardiovasc Prev (2010) 17: 201. doi:10.2165/11311960-000000000-00000


Arterial hypertension is a main cause of cardiac remodelling, which is characterized by left ventricular hypertrophy and diastolic dysfunction. Cardiac remodelling is associated with modifications of the extracellular matrix. The molecular structure of the extracellular matrix is controlled by proteolytic enzymes called matrix metalloproteinases (MMPs), which degrade collage, elastin, fibronectin and proteoglycans. The activity of MMPs is modulated by their natural inhibitors, the tissue inhibitors of MMPs (TIMPs), which bind the MMPs, preventing their proteolytic action. In hypertension, MMPs and TIMPs may contribute to cardiac remodelling by altering the composition of the extracellular matrix. Clinical studies in hypertensive patients have shown modulation of plasmatic concentration of MMPs and TIMPs. Also, plasmatic concentration of MMPs and TIMPs seem to be predictive of left ventricular hypertrophy, diastolic dysfunction and heart failure in hypertensive patients. However, the different technical approaches as well as the complexity of the MMP/TIMP system render it difficult to get a consensus on the pattern of their plasmatic changes in hypertension. These limitations might be overcome by large and prospective additional studies, providing a definite answer about the role of plasmatic MMPs and TIMPs as biomarkers of cardiac remodelling in hypertensive patients.


biomarkersdiastolic dysfunctionextracellularleft ventricular hypertrophy

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