Inhibiting extracellular matrix metalloproteinase inducer maybe beneficial for diminishing the atherosclerotic plaque instability.(Viewpoint essay)

Byline: S. Xie, R. Nie, J. Wang

Atherosclerotic plaque rupture and local thrombosis activation in the artery cause acute serious incidents such as acute coronary syndrome and stroke. The exact mechanism of plaque rupture remains unclear but excessive degradation of the extracellular matrix scaffold by matrix-degrading metalloproteinases (MMPs) has been implicated as one of the major molecular mechanisms in this process. Convincing evidence is available to prove that extracellular matrix metalloproteinase inducer (EMMPRIN) induces MMP expression and is involved in the inflammatory responses in the artery wall. The inflammation and MMPs have been shown to play a critical role for atherosclerotic lesion development and progression. More recent data showed that increased EMMPRIN expression was associated with vulnerable atherosclerotic lesions. Therefore, we speculate that EMMPRIN may be pivotal for atherosclerotic plaque instability, and hence inhibition of EMMPRIN expression could be a promising approach for the prevention or treatment of atheroma instability.

Acute coronary syndrome (ACS) and stroke are clinical events that cause considerable immediate morbidity and mortality. The rupture of vulnerable atherosclerotic plaque represents a key process that often leads to ACS or stroke.[sup] [1] Over the past several years, it has been recognized that plaque composition such as inflammatory cells and lipid-core plays a more important role than plaque size or stenosis severity in plaque rupture and thrombosis. Convincing evidences have demonstrated that MMPs contribute to the extracellular matrix loss in the fibrous cap and have been implicated in promoting the plaque rupture and the related vascular events.[sup] [2],[3],[4],[5],[6] Particular interests have been focused on the role …