MRGD Deficiency Leads to Dilated Cardiomyopathy

What are the cardiac effects of genetic deletion of the alamandine peptide receptor MRGD? Listen as Associate Editor Debra Diz (Wake Forest University School of Medicine) interviews lead author Robson Santos (Universidade Federal De Minas Gerais, Brazil) and content expert Michelle Parvatiyar (Florida State University) about the innovative work by Oliveira et al. Santos and co-authors found that genetic deletion of MRGD in mice triggered the development of severe dilated cardiomyopathy in the absence of hypertension. Robson and colleagues found several key phenotypic changes—increased adiposity chief among them—but no changes in blood pressure in the MRGD knockout mice. Surprisingly the authors found a decrease in ANP expression, leading them to consider ANP key to the pathogenesis of the cardiac dysfunction in this animal model. Don’t miss the behind-the-scenes story of how alamandine got its unique name. Listen now.

 

Aline Cristina Oliveira, Marcos Barrouin Melo, Daisy Motta-Santos, A Augusto Peluso, Fernando Souza-Neto, Rafaela F da Silva, Jonathas FQ Almeida, Giovanni Canta, Adelina M. Reis, Gleisy Goncalves, Gabriela G Cerri, Danielle Coutinho, Itamar Couto Guedes de Jesus, Silvia Guatimosim, Natalia D Linhares, Natalia Alenina, Michael Bader, Maria José Campagnole-Santos, and Robson A. Souza Santos Genetic deletion of the alamandine receptor MRGD leads to dilated cardiomyopathy in mice Am J Physiol Heart Circ Physiol, published January 8, 2019. DOI: 10.1152/ajpheart.00075.2018

Differential Control of Sympathetic Outflow in Young Humans

What drives variability in muscle sympathetic nerve activity among healthy individuals? Associate Editor Nisha Charkoudian (U.S. Army Research Institute of Environmental Medicine) explores this central question in a new interview with lead author Philip Millar (University of Guelph) and content expert Craig Steinback (University of Alberta) about the work by Incognito et al. Millar and co-authors identified subpopulations within muscle sympathetic single unit nerve fibers that display opposite responses to typical sympathoexcitatory stressors-- lower body negative pressure and an exercise stimulus. The authors uncovered that we can recruit, and de-recruit, individual muscle sympathetic nerve fibers in response to these stressors. What are the potential clinical implications for patients with orthostatic intolerance or hypertension? Listen to find out.

 

Anthony V. Incognito, Connor J. Doherty, Massimo Nardone, Jordan B. Lee, Karambir Notay, Jeremy D. Seed, and Philip J. Millar Evidence for differential control of muscle sympathetic single units during mild sympathoexcitation in young, healthy humans Am J Physiol Heart Circ Physiol, published December 17, 2018. DOI: 10.1152/ajpheart.00675.2018