Complement and atherogenesis: The unknown connection

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Abstract
The question why low-density lipoprotein (LDL) stranded in the subendothelium of arteries should acquire the proinflammatory properties that initiate and sustain atherogenesis has puzzled researchers for decades. The most popular concept contends that oxidative processes are crucial because oxidized LDL (ox-LDL) produced in vitro has atherogenic properties and small amounts of it are found in atherosclerotic lesions. Recently, a possible role for vascular infections has also been considered because infectious agents, in particular Chlamydia pneumoniae, are sometimes present in the lesions. Here, evidence is summarized for a different concept of atherogenesis, which evolves from the fact that nonoxidative, enzymatic degradation of LDL transforms the lipoprotein to an atherogenic moiety. Our group proposes that enzymatically degraded LDL (E-LDL) initiates and sustains atherosclerosis through its capacity to activate complement and macrophages. These processes are initially meaningful because they enable the stranded lipoprotein to be removed from the vessel wall, but they become harmful when the cholesterol removal system is overloaded. A novel type of chronic inflammation then ensues producing the characteristic pathology of the atherosclerotic lesion.

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