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The molecular mechanisms of the thrombotic complications of atherosclerosis
Author(s) -
Libby P.
Publication year - 2008
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2008.01965.x
Subject(s) - medicine , thrombosis , pathophysiology , matrix metalloproteinase , fibrous cap , vulnerable plaque , oxidative stress , coronary artery disease , pathogenesis , disease , bioinformatics , pathology , cardiology , biology
Our evolving knowledge of the cellular and molecular mechanisms underlying atherosclerosis has helped uncover the underlying causes behind thrombotic complications of this disease. Most fatal coronary thrombosis result from fibrous cap rupture or superficial erosion. Recent research has established a role for matrix metalloproteinases in the regulation of aspects of plaque structure related to propensity to disrupt and provoke thrombosis. Inflammatory pathways impinge on proteinase activity and aspects of oxidative stress that may favour plaque disruption. Novel molecular imaging strategies may permit visualization of proteinase activity in vivo , providing a new functional window on pathophysiology.