Download The Anitschkow Prize in Atherosclerosis Research, 2013

European Atherosclerosis Society
Kronhusgatan 11, SE-411 05, Göteborg, SWEDEN, Tel: +46(0)31 724 27 95,
Fax: +46(0)31 724 27 01, E-mail: [email protected]
The Anitschkow Prize in Atherosclerosis
Research, 2013
The EAS is delighted to announce that the recipient of the Society's
prestigious Anitschkow Prize 2013 (Diploma+10000 EUR) is Professor Peter
Libby, Mallinckrodt Professor of Medicine at Harvard Medical School and
Chief of the Cardiovascular Division at Brigham and Women's Hospital,
Boston, Massachusetts.
The Anitschkow Prize Recipient 2013
Here you can read more about Prof. Peter Libby's major discoveries.
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Prof. Libby discovered that vascular wall cells can produce pro-inflammatory cytokines
as well as respond to them. This discovery suggested autocrine and paracrine cytokine
inflammatory signaling in arterial disease, and laid the groundwork for a new field in
atherosclerosis research for laboratories worldwide. Prof. Libby used genetic and
antibody-mediated loss of function in mice to establish roles for cytokines in
atherosclerosis.
Prof. Libby originated the concept that the dynamic metabolism of arterial collagen
regulated by inflammatory signals governed the susceptibility of atherosclerotic plaques
to disruption and thrombosis. He discovered the inhibition by Th1 cytokines of collagen
production by human smooth muscle cells and the overexpression of interstitial
collagenases (MMPs 1, 8, 13) in human atheromata. He showed that inhibition of these
enzymes can strengthen the atheroma by increasing its collagen content. He also showed
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that lipid-lowering can exert anti-inflammatory actions and ameliorate properties of
plaques linked to thrombotic complications. This sustained series of discoveries furnished
the foundation for current thinking about the molecular basis of the acute coronary
syndromes, and the mechanism of benefit of therapies that reduce risk of myocardial
infarction and stroke.
In 1989 Prof. Libby proposed a model for the immunopathogenesis of transplantation
arteriopathy. His later experiments in genetically altered mice proved his original
postulates of an alloimmune response to donor vascular cells with a central role of
signaling due to interferon-gamma. This model has gained wide acceptance, and provided
the foundation for much subsequent research and clinical progress in this field.
In 1993 Prof. Libby showed sustained inflammatory activation of vascular cells
following arterial injury. At that time, the hypotheses of the pathogenesis of restenosis
after arterial intervention highlighted thrombosis and arterial smooth muscle cell
proliferation. Prof. Libby’s pioneering discovery of the operation of inflammation
pathways after arterial injury laid the scientific foundation for the clinical success of the
immunosuppressive agents in drug-eluting stents.
Prof. Libby has recently elucidated a mechanism that explains the dimorphic expression
of atherosclerosis; sometimes stenotic and sometimes aneurysmal. In a landmark
publication Prof. Libby showed a Th1-skewed response in typical atherosclerosis but a
predominant Th2 response in human aortic aneurysmal disease. Subsequent work in
genetically altered mice has substantiated the concept that Th1/Th2 balance plays a key
role in the pathogenesis of arterial aneurysms.
Prof. Libby has contributed pivotally to the molecular imaging of vascular inflammation.
In particular, his laboratory has established and validated techniques that visualize the
activity of the matrix metalloproteinases which he had previously shown to be produced
by inflammatory cells in atherosclerotic plaques. These proteinases degrade arterial
collagen, weaken the fibrous plaques, and thus heighten the risk of the thrombotic
complications of atherosclerosis.
Finally, Prof. Libby has fostered the rapid translation to the clinic of the concepts of
inflammation in arterial pathophysiology that emerged from his own laboratory work
over the last twenty years. He has championed the concept that inflammation provides a
mechanistic link between classical risk factors such as dyslipidemia and altered arterial
biology. He has inspired, enabled, and participated in a number of the clinical studies that
have placed inflammation at the forefront of current thinking about the diagnosis, risk
stratification, and therapeutic approaches to atherosclerotic cardiovascular disease.
Professor Libby's Anitschkow Lecture is available to view as a webcast on the EAS
Academy. Log in to view.