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.
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