title: Basic science for the clinician 44: atherosclerosis: an immunologically mediated (autoimmune?) disease.
abstract: There has been a sea change in our understanding of atherosclerosis. We have come a long way from the days where eating too much fat and not getting enough exercise and having the wrong genetic background was thought to be the entire story. A few years ago, the cardiologists began to embrace inflammation as a possible pathogenetic mechanism and from that came high-sensitivity C-reactive protein testing for just about everyone. Chronic systemic inflammation became an area of interest. We have learned that it is more than just corticosteroid use that causes accelerated atherosclerosis in our rheumatoid and lupus patients. Even C-reactive protein may be a pathogenetic player, not only a diagnostic clue. Oxidized phospholipids and the cells that recognize them may be crucial in the evolution of the atherosclerotic plaque. Statins may be useful in suppressing inflammation, not only in suppressing cholesterol levels. And now even cardiologists are thinking about immune mechanisms! A strange world, but the beneficiaries of going through this looking glass will be our patients. A true understanding of this seems to have required a most circuitous route-sometimes you have to leave for a long journey before you can return and really see home for the first time.
authors.affiliation: Research and Development, Bristol-Myers Squibb, Princeton, NJ, USA. leonard.sigal@bms.com
authors.forename: Leonard H
authors.initials: LH
authors.lastname: Sigal
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000276:immunology* / Q000503:physiopathology; D001323:Autoantibodies / Q000097:blood; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000503:physiopathology; D008075:Lipoproteins, HDL / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D010084:Oxidation-Reduction
chemical_list: D001323:Autoantibodies; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL