Abstract
Myocardial diseases and atherosclerosis are widely considered to be an immune mediated process. Fcγ receptors (FcγRs) contribute to the regulation of immune and inflammatory responses and have been implicated in human cardiovascular lesions. Major cell types involved in the pathogenesis of the diseases express FcγRs and their ligands such as immune complexes and C-reactive protein have been shown to activate FcγRs signal pathway. This review summarizes recent significant progress addressing the various roles of FcγRs in the disease pathogenesis which comes from the studies of FcγRs deficient animal models, clinical investigations and in vitro molecular and cellular studies. These new findings help us appreciate the emerging role of FcγRs in cardiovascular diseases, and suggest FcγRs as a potential therapeutic target for the diseases.
Highlights
It is well established that myocardial diseases and atherosclerosis are inflammatory diseases of the myocardium and the wall of largeand medium-sized arteries where both innate and adaptive immunity response play a pivotal role in the initiation, growth and progress of the lesions [1]
These results suggest that the formation and interaction of immune complexes of LDL with Fcγ receptors (FcγRs) on monocytic cells is involved in the generation of macrophage-derived foam cells
SFcγRIIIaMΦ level in the plasma was correlated with carotid maximum intima-media thickness and a number of risk factors for atherosclerosis: such as aging, current smoking, diabetes, hypertension, LDL-cholesterol to HDL-cholesterol ratios, and family history of atherosclerotic diseases in subjects undergoing an annual medical checkup [59]. These findings indicate that the macrophages are activated during the process of atherosclerosis, and sFcγRIIIaMΦ might serve as a novel biomarker for atherosclerosis
Summary
It is well established that myocardial diseases and atherosclerosis are inflammatory diseases of the myocardium and the wall of largeand medium-sized arteries where both innate and adaptive immunity response play a pivotal role in the initiation, growth and progress of the lesions [1]. Increasing lines of evidence suggest that FcγRs are implicated in the pathogenesis of myocardial diseases and atherosclerosis. Immune complexes may form between these antigens and autoantibodies and promote the progression of the disease via FcγRs cross-linkage and activation and complement activation [9]. C-reactive protein, a crucial mediator of cardiovascular disease, elicits a wide array of harmful effects in a majority of cell types involved in the disease pathogenesis, mostly mediated via Fcγ receptor-dependent pathways [10]. In this review we will summarize recent studies addressing the multifaceted roles of FcγRs in cardiovascular diseases
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