Background: Atherosclerosis and its complications represent the leading cause of morbidity and mortality. Heat shock protein 70 (HSP70) protects cellular elements from injury by reducing oxidation, inflammation and apoptosis and by refolding damaged proteins. HSP70 improves viability of stressed vascular smooth muscle cells, possibly via its chaperone functions. It has been proposed that the response mounted against bacterial HSPs results in an autoimmune reaction, which has the potential to cause complement-mediated endothelial injury, and hence accelerate atherogenesis.
Objective: to examine the roles of HSPs in atherosclerosis.
Methods: A literature review.
Results/conclusions: The role of HSPs in atherosclerosis is controversial. HSP60 probably acts as an autoantigen, and may trigger both cell- and antibody-mediated immune responses, while HSP70 is likely to be involved in cytoprotection. The significance of this inverse relation between HSP70 and atherosclerosis has not yet been elucidated. Whether HSPs will become therapeutic targets remains to be established.