Dr. Hope Anderson is a Professor of Pharmacy with a cross-appointment in the Department of Pharmacology and Therapeutics in the College of Medicine. The goal of her research program is to understand how risk factors for cardiovascular disease, especially hypertension (high blood pressure), cardiac hypertrophy (abnormal growth of the heart), and diabetes promote the development of heart failure. Her ultimate aim is to identify new therapies that prevent or slow the onset of heart failure. To achieve this aim, Dr. Anderson’s laboratory uses several models of cardiovascular disease of escalating complexity ranging from cultured heart muscle cells, to isolated hearts and arteries, to hearts and arteries in vivo.
A significant interest of the lab is novel signaling mechanisms that underlie cardiac hypertrophy. One important example is our focus on the endocannabinoid system as a therapeutic target to achieve protection of the heart after hemodynamic stress or injury. This CIHR-funded project led to the discovery that activating cannabinoid receptors results in stimulation of signalling pathways that prevent abnormal growth of the heart. Moreover, the activated endocannabinoid system leads to protection of mitochondria in heart muscle cells. Mitochondria are responsible for generating energy; since heart muscle cells contract and relax constantly (and this requires a continuous supply of energy), mitochondria are very important. We are currently extending our findings on the cardioprotective actions of CB receptors to the major clinical challenge of atrial fibrillation, a type of irregular heartbeat. To do this, we are collaborating with Dr. Yoram Etzion (Ben-Gurion University, Israel), with support through a St. Boniface Hospital – Ben-Gurion University Research without Borders Operating Grant. Dr. Etzion has developed innovative technology to study atrial fibrillation in experimental models, which we will leverage here in the College of Pharmacy to interrogate cannabinoid receptor-mediated effects.
The role of resistance arteries in hypertension is another important focus of the lab. Blood pressure is influenced by peripheral resistance to blood flow, and resistance increases as the arterial lumen diameter narrows (whether by structural, functional, and/or mechanical mechanisms). An important therapeutic aim, for which we are testing nutritional interventions, is to prevent this narrowing. In past years, we reported the microvascular (and cardiac) effects of resveratrol. Resveratol is a stilbenoid polyphenol that became popular after putative links to benefits such as increased longevity. There is, in fact, a significant body of evidence that resveratrol might be protective in the context of cardiovascular disease. However, resveratrol exhibits low oral bioavailability and a short half-life. Thus, we are focusing on protective effects of stilbenoid compounds with improved bioavailability (i.e. pterostilbene, a dimethylated analog of resveratrol) or a history of medicinal use (i.e. gnetol) on arteries and the heart in the spontaneously hypertensive heart failure (SHHF) rat, an experimental model of human hypertension and heart disease.
Another project in the lab is predicated on our hypothesis that aberrations of brain-penetrating arterioles contribute to cerebral vascular insufficiency in the context of cardiovascular disease, and that this potentiates the risk of cognitive decline and dementia during heart failure. We are characterizing these aberrations using a combination of pressure myography and multi-photon laser scanning microscopy in isolated arteries and brain slices, assessing the effects of mechanical strain, and interrogating signaling effectors.
Ph.D., Pharmacology & Therapeutics, University of Manitoba.
B.Sc., Microbiology, with Honours, University of Manitoba.
For a current list -
Hope Anderson, Ph. D.