Abstract
Heat Shock Proteins (HSPs) are a group of highly conserved molecular chaperones that play important roles in homeostasis and the cellular response to stress. In the cardiovascular system, HSPs maintain vessel wall integrity and cardiomyocyte function; they may be upregulated and translocated to the cell surface in response to environmental stressors. HSPs contribute to the inflammatory processes that mediate the development of atherosclerosis by activating the innate and adaptive immune response. Misdirected autoimmune attack of surface HSPs on stressed vascular endothelial cells by circulating anti-Hsp60 antibodies lead to damage of the vessel wall and atherogenesis. Additionally, other HSPs contribute to the pro-inflammatory state in the vessel wall by stimulating macrophages and reactive Tcells to release cytokine and chemotactic factors. Atrial Fibrillation (AF) is closely related to atherosclerotic burden and changes to levels of various HSPs have been associated with increased incidence of AF in stressed cardiomyocytes after ischemia reperfusion injury. Modulation of HSP expression may be a useful therapeutic strategy in the management of atherosclerosis and AF.
Keywords: Heat shock proteins, HSP, HSP60, autoimmunity, atherosclerosis, atrial fibrillation.
Graphical Abstract
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