Stress proteins and atherosclerosis.
Several cytotoxic stimuli of a different nature are involved in the complex etiology of atherosclerosis. Cells of the vasculature may potentially cope with the presence of these stressors through the increased synthesis of stress proteins (or heat shock proteins, hsps), an ubiquitous and conserved defense response. Evidence exists that the expression of two stress proteins of intermediate molecular weight, hsp60 and hsp70, is higher at sites of atherosclerotic lesions than it is in normal tissue. The role of hsps in atherosclerosis is controversial. While hsp70 is likely to be involved in cytoprotection, hsp60 is probably acting as an autoantigen, and may trigger both cell-mediated and antibody-mediated immune responses.
Roma
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Institute of Pharmacological Sciences, University of Milano, Italy.
Catapano
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D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000276:immunology / Q000378:metabolism; D018834:Chaperonin 60 / Q000502:physiology; D018840:HSP70 Heat-Shock Proteins / Q000502:physiology; D006360:Heat-Shock Proteins / Q000502:physiology*; D006801:Humans; D012307:Risk Factors
D018834:Chaperonin 60; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins