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