Reema Flynn-Rizk
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Reema Flynn-Rizk has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Andrew McClennan
Imaging Program, Lawson Research Institute/SJHC, London, ON N6C 2R5, Canada
1 shared publication - Anish Chhabra
Imaging Program, Lawson Research Institute/SJHC, London, ON N6C 2R5, Canada
1 shared publication - Carlie Charron
Dalhousie University
1 shared publication - Leonard G. Luyt
The University of Western Ontario 1151 Richmond St
1 shared publication - Lisa M. Hoffman
Imaging Program, Lawson Research Institute/SJHC, London, ON N6C 2R5, Canada
1 shared publication - Maedeh Naghibosadat
Sunnybrook Health Sciences Centre, Toronto, ON M4N 3M5, Canada
1 shared publication
Latest Publications
- Open Access
Growth Hormone Secretagogue Receptor (GHSR) Is Elevated in Myocardial Tissues of DMD mdx:utrn−/− Mice, and Correlates Strongly with Inflammatory Markers, and Negatively with Cardiac Function
Dilated cardiomyopathy affects greater than 1 in 2500 patients worldwide, including those with the neuromuscular disorder Duchenne muscular dystrophy (DMD). While inflammation within skeletal muscle is strongly associated with DMD pathology, the key biomarkers for inflammation and possible targets for therapy within cardiac tissue in DMD-associated dilated cardiomyopathy remain to be identified. One such potential target is the myocardial ghrelin-growth hormone secretagogue receptor (GHSR) system, which is associated with cardiomyocyte survival and inhibition of inflammation. We sought to determine alterations in myocardial GHSR together with markers of cardiac inflammation using mdx:utrn−/− mice as a model for DMD-associated dilated cardiomyopathy. With traditional histopathology, we determined that the pathology of DMD in mdx:utrn−/− mice was characterized by disruption of myofiber organization, lymphocytic infiltration, and extensive cardiomyocyte vacuolization and necrosis surrounding areas of fibrosis in the left ventricular wall and apex. Using a fluorescent ghrelin analog, Cy5-ghrelin (1–19), to visualize GHSR with fluorescence confocal microscopy, we demonstrate that GHSR is elevated in mdx/utrn−/− myocardial tissues and correlates strongly with both F4-80 (activated macrophages) and IL-6 (pro-inflammatory cytokine), and negatively with cardiac function. We also show that GHSR can be visualized in pro-inflammatory macrophages, suggesting a direct role for GHSR in the inflammatory progression of DMD.
Open AccessGrowth Hormone Secretagogue Receptor (GHSR) Is Elevated in Myocardial Tissues of DMD mdx:utrn−/− Mice, and Correlates Strongly with Inflammatory Markers, and Negatively with Cardiac Function
Dilated cardiomyopathy affects greater than 1 in 2500 patients worldwide, including those with the neuromuscular disorder Duchenne muscular dystrophy (DMD). While inflammation within skeletal muscle is strongly associated with DMD pathology, the key biomarkers for inflammation and possible targets for therapy within cardiac tissue in DMD-associated dilated cardiomyopathy remain to be identified. One such potential target is the myocardial ghrelin-growth hormone secretagogue receptor (GHSR) system, which is associated with cardiomyocyte survival and inhibition of inflammation. We sought to determine alterations in myocardial GHSR together with markers of cardiac inflammation using mdx:utrn−/− mice as a model for DMD-associated dilated cardiomyopathy. With traditional histopathology, we determined that the pathology of DMD in mdx:utrn−/− mice was characterized by disruption of myofiber organization, lymphocytic infiltration, and extensive cardiomyocyte vacuolization and necrosis surrounding areas of fibrosis in the left ventricular wall and apex. Using a fluorescent ghrelin analog, Cy5-ghrelin (1–19), to visualize GHSR with fluorescence confocal microscopy, we demonstrate that GHSR is elevated in mdx/utrn−/− myocardial tissues and correlates strongly with both F4-80 (activated macrophages) and IL-6 (pro-inflammatory cytokine), and negatively with cardiac function. We also show that GHSR can be visualized in pro-inflammatory macrophages, suggesting a direct role for GHSR in the inflammatory progression of DMD.