Focus on EAS Innsbruck 2016: Introducing the faculty - Plenary speaker Assam El-Ost
02 November 2015
A forward-looking scientific Programme to excite, inspire and inform!
The EAS 2016 Scientific Committee has created a programme featuring ground-breaking speakers in their respective fields. EAS 2016 Innsbruck welcomes a distinguished international faculty to share their forward-looking perspectives on the latest developments in basic research and clinical practice in atherosclerosis and cardiovascular disease. You can find details of the Plenary and Workshop sessions now on the Congress website, www.eas2016.kenes.com.
Abstract submission is now open. Submit your abstract by January 11, 2016 for the opportunity to present your findings at this prestigious international Congress.
Here, in a series of newsletters, we introduce members of the EAS 2016 Innsbruck faculty.
Plenary session 1, Monday, May 30, 2016: Integrative approach in atherosclerosis
Assam El-Osta, Australia: Epigenetics in atherosclerosis
Dr Assam (Sam) El-Osta is an NHMRC Senior Research Fellow, Head of the Epigenetics in Human Health and Disease Laboratory (incorporating the Epigenomics Profiling Facility) at Baker IDI, Heart and Diabetes Institute, and Professor of Medicine, Monash University, Melbourne, Australia. His research has contributed to understanding the molecular mechanisms whereby epigenetic changes exert positive and negative transcriptional functions in specific model systems, in particular understanding the roles of specific components of regulatory complexes in the regulation of metabolic memory and cardiac hypertrophy. Dr El-Osta is the recipient of numerous awards, including the Australian Society for Medical Research AMGEN 'Australian Medical Researcher of the Year' and Juvenile Diabetes Research Foundation/Macquarie Group Foundation 'Diabetes Research Innovation Award for an Early Career Researcher'.
Elucidation of epigenetic mechanisms, such as those involving DNA methylation and deacetylation, and histone modification, has significantly enhanced understanding of the pathogenesis of atherosclerosis. Importantly, such epigenetic processes are flexible genomic factors that not only allow a change in genome function with external influences, but also stable propagation of gene expression. Both cell-specific gene expression and environment-mediated changes in expression patterns can be explained by a complex network of modifications to the DNA, histone proteins and the degree of DNA packaging.
Moreover, it is increasingly appreciated that gene-environment interactions, especially in the context of human health and disease, involve epigenetic pathways, and that epigenetic patterns may change in response to environmental exposure or nutritional status. Specific epigenetic influences of dietary glucose and lipid consumption, as well as undernutrition, are observed across numerous organs and pathways associated with metabolism. Recent studies have shown that gene regulation underlying phenotypic determinants of adult metabolic health is influenced by maternal and early postnatal diet.
These emerging concepts suggest new therapeutic potential for targeting the epigenome. Both in vitro and in vivo studies using drugs targeting enzymes involved in epigenetic modifications have shown considerable promise in atherosclerosis treatment. For example, identification of histone deacetylase inhibitors in animal models may offer novel treatments for atrial fibrillation, cardiac hypertrophy and heart failure. Importantly, cardiovascular epigenomics research may also offer opportunities to combat the escalating pandemic of cardiometabolic disease.
Keating ST, El-Osta A. Epigenetics and metabolism. Circ Res 2015;116:715-36
Mathiyalagan P, Keating ST, Du XJ, El-Osta A. Interplay of chromatin modifications and non-coding RNAs in the heart. Epigenetics 2014;9:101-12.
Mathiyalagan P, Keating ST, Du XJ, El-Osta A. Chromatin modifications remodel cardiac gene expression. Cardiovasc Res 2014;103:7-16.