The Robert Roberts Award, in recognition of the pioneering cardiovascular research of Dr. Robert Roberts (Heart Institute CEO from 2004-2014), recognizes an Institute Investigator who published in the preceding year a peer-reviewed, original research paper that has a high impact on cardiovascular science.
In 2016 two publications made the cut and two awards were given out by the selection committee on May 30th at the Institute’s Research Day. The recipients for 2016 were Dr. Ruth McPherson (MD) and Dr. Katey Rayner (PhD).
Dr. Ruth McPherson, Director of the Ruddy Canadian Cardiovascular Genetics Centre received the prize for leading a landmark collaborative study that was published in the prestigious journal Nature Genetics. The study described a comprehensive survey of the fine genetic architecture of cardiovascular disease, showing that genetic susceptibility to heart disease is largely determined by the cumulative effects of numerous small genetic variants. This study represented a collaboration within the international CARDIOGRAM Plus 4D Consortium and was led by researchers at the University of Oxford in the UK, the Broad Institute of MIT and Harvard University and the Ottawa Heart Institute and involved a total of 48 centres around the world including more than 185,000 individuals.
The publication can be found at the Nature Genetics website: A comprehensive 1,000 Genomes-based genome-wide association
Dr. Katey Rayner and the research team in the Cardiometabolic microRNA Laboratory received the prize for their study published in Circulation Research examining microRNAs, which are tiny genetic material that can have major downstream effects on cellular functions and disease processes. The current study uncovered a major role for a microRNA, called miR-33, in the atherosclerotic disease process. The team showed that miR-33 plays a central role in LDL (i.e. bad cholesterol) accumulation in the artery wall. When the team experimentally blocked the action of miR-33, the cells had an increased ability to remove cholesterol buildup, by a mechanism that involved the cells’ mitochondria or energy supply.
The study also found that the amount of miR-33 in arteries from patients suffering from atherosclerosis, is elevated compared to those with healthy arteries, and that the pathways that control mitochondria energy production were decreased. There is major potential to ultimately treat patients with atherosclerosis with inhibitors of miR-33, or anti-miR33, to boost the mitochondrial energy supply, promote cholesterol removal from the arteries and prevent heart attacks. Other microRNA inhibitors are in advanced Phase III clinical trials for chronic diseases like Hepatitis C, so there are high hopes for this class of drugs for the future.
The publication can be found at the Circulation Research website: Macrophage Mitochondrial Energy Status Regulates Cholesterol Efflux and Is Enhanced by Anti-miR33 in Atherosclerosis