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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:2205.)
© 2004 American Heart Association, Inc.

Editorials

Proteolysis of Pericellular Matrix

A Process Linking Inflammation to Plaque Destabilization and Rupture

Ken A. Lindstedt; Petri T. Kovanen

From the Wihuri Research Institute, Helsinki, Finland.

Correspondence to Petri T. Kovanen, Wihuri Research Institute, Kalliolinnantie 4 FI-00140, Helsinki, Finland. E-mail petri.kovanen@wri.fi

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The two major general cellular concepts in atherogenesis, foam cell formation and growth of smooth muscle cells (SMCs) in the arterial intima, have not been able to satisfactorily explain the evolution of advanced complex atherosclerotic lesions behind acute atherothrombotic events leading to acute coronary syndromes. Rather, in terms of intimal pathophysiology, the two above cellular processes can be considered beneficial and homeostatic, the formation of foam cells resulting in clearance of toxic substances from the tissue, and growth of SMCs strengthening it. The basic pathology behind the acute coronary syndromes, again, relates to rupture of unstable coronary plaques consisting of a large extracellular necrotic lipid and a thin fibrous cap covering it. At the cellular level, a switch from cell growth to cell death, notably to apoptosis, may be involved in transforming a stable plaque into an unstable one. Thus, death of foam cells likely contributes to the formation of the necrotic lipid core, and death of SMCs to cap remodeling with ensuing formation of a thin and vulnerable cap. Stromal cells, such as the intimal SMCs, need an intact matrix environment for normal function and survival. Hence, also the vulnerability of an atherosclerotic plaque may critically depend on the integrity of the peri- and extracellular matrices of the plaque SMCs.^1,2 In vitro studies have revealed that plaque-infiltrating inflammatory cells, such as macrophages and mast cells, are capable of secreting a variety of proteolytic enzymes. Some of them can degrade peri- and extracellular matrix components either directly or indirectly by . . . [Full Text of this Article]

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