Anitschkow Prize Recipient 2020

EAS is pleased to announce Professor Joseph L. Witztum,
San Diego, USA as the recipient of the Anitschkow Award 2020.
This prestigious Prize, awarded annually by the EAS, recognizes outstanding research in the field of atherosclerosis and linked metabolic disturbances.
The 2020 award recognizes the exceptional contributions of Professor Witztum in providing a fundamental understanding of the role of oxidized low-density lipoproteins (LDL) and immunological mechanisms in atherogenesis.

About the Winner

Professor Witztum is the Distinguished Professor of Medicine at the University of California, San Diego, USA. He is also Associate Editor of major scientific journals in the field of atherosclerosis research, and in 2016, stepped down after 13 years as the Editor-in-Chief of the Journal of Lipid Research. Professor Witztum received his Bachelor’s Degree from Vanderbilt University, where he graduated magna cum laude, and an MD from the Washington University School of Medicine in St. Louis. He completed his internship and residency in Internal Medicine at Mt. Sinai Hospital in New York City, followed by a fellowship and faculty position in Endocrinology and Metabolism at Washington University School of Medicine. He has been at the University of California, San Diego since 1979.

In addition, Professor Witztum has contributed to atherosclerosis research as an excellent mentor, training many scientists who are now well-recognised professors in Universities worldwide.

About Professor Witztum’s Research

Professor Witztum started his career more than four decades ago with studies in human hyperlipidemias and clinical trials. He then made a seminal contribution with the late Dr. Daniel Steinberg in formulating the “oxidation hypothesis” of atherosclerosis, based on the discovery that oxidized LDL is taken up by scavenger receptors resulting in foam cell formation. Further work documented the presence of oxidized LDL in atherosclerotic lesions in humans and identified several biological activities of these modified lipoprotein particles and their components, providing mechanistic insights into the disease process. The oxidation hypothesis is now considered one of the major concepts for the pathogenesis of atherogenesis.

Subsequent discoveries by Dr. Witztum showed that oxidized LDL is immunogenic and has the capacity to trigger antibody responses. His research demonstrated that oxidation-specific epitopes are endogenous danger-associated molecular signals that trigger innate and adaptive immune responses. These insights have provided a rationale for new approaches aimed at modulating immunological responses to prevent or treat atherosclerosis-related diseases. His recent work has extended to lipoprotein(a) and its role as a carrier of oxidation-specific epitopes in humans.

Professor Witztum recently achieved a major breakthough in establishing the role of oxidized phospholipids as mediators of the pathogenic effects of oxidized LDL. His laboratory previously identified the immunoglobulin natural antibody E06, which binds oxidized phospholipids and neutralizes their proinflammatory activities in vitro. His laboratory created a novel mouse model that expresses a single chain variant of this antibody under the control of apolipoprotein E regulatory elements. When crossed with LDL receptor deficient mice, expression of the single chain E06 antibody dramatically reduced atherosclerosis, reduced macrophage foam cell formation, and significantly reduced molecular and biochemical markers of inflammation. These findings, published in Nature, (see reference 1 below) clearly underline the role of oxidized LDL, oxidation-specific epitopes and subsequent pathological pathways in atherogenesis and have important translational implications.


1. Que X, Hung MY, Yeang C, Gonen A, Prohaska TA, Sun X, Diehl C, Määttä A, Gaddis DE, Bowden K, Pattison J, MacDonald JG, Ylä-Herttuala S, Mellon PL, Hedrick CC, Ley K, Miller YI, Glass CK, Peterson KL, Binder CJ, Tsimikas S, Witztum JL. Oxidized phospholipids are proinflammatory and proatherogenic in hypercholesterolaemic mice. Nature 2018;558:301-306. PUBMED