July 27, 2017
Do the well-established beneficial effects of EETs (epoxyeicosatrienoic acids) in the vasculature also extend to the myocardium? That's just what we explore in this new podcast about the work by Cao et al, which is highlighted in our Call for Papers on Heart Failure - Novel Therapeutic Pathways Emerging from Basic Science. Listen as Consulting Editor David D. Gutterman (Medical College of Wisconsin) interviews lead author Nader G. Abraham (New York Medical College) and content expert Kevin Dellsperger (Augusta University Health System) about the translational work by Abraham and colleagues. As a downregulator of NOV, EETs act as anti-inflammatory molecules attenuating cardiac damage. Abraham and co-authors found that EETs increase Wnt, resulting in the reprogramming of epicardial fat toward a brown fat phenotype, thereby increasing left ventricle function and contractility. What novel and "potentially drug-able" pathway is responsible for attenuating obesity-induced cardiomyopathy? Listen now.
Jian Cao, Shailendra P. Singh, John McClung, Gregory Joseph, Luca Vanella, Ignazio Barbagallo, Houli Jiang, John R. Falck, Michael Arad, Joseph I. Shapiro, Nader G. Abraham EET Intervention on Wnt1, NOV and HO-1 Signaling Prevents Obesity-Induced Cardiomyopathy in Obese Mice Am J Physiol Heart Circ Physiol, published June 2, 2017. DOI: 10.1152/ajpheart.00093.2017
July 25, 2017
Does the branch chain amino acid leucine mediate cardiac insulin resistance? Listen as Associate Editor Gary Lopaschuk (University of Alberta) interviews lead author Luc Bertrand (Université Catholique de Louvain) and content expert Ravichandran Ramasamy (NYU Langone Medical Center) about the recent work by Renguet et al which investigated whether leucine is simply a biomarker of type 2 diabetes or a factor of the metabolic inflexibility which is a hallmark of type 2 diabetes pathogenesis. Bertrand and colleagues showed that the inhibitory reaction of leucine and ketone bodies in glucose transport requires an increase in protein acetylation, which then contributes to the inhibition of cardiac glucose uptake by hampering the translocation of glucose transporter 4 (GLUT4) to the plasma membrane. This new study by Bertrand and colleagues may be “a new piece in the complex puzzle of cardiac insulin resistance.” Listen and learn more.
Edith Renguet, Audrey Ginion, Roselle Gélinas, Laurent Bultot, Julien Auquier, Isabelle Robillard Frayne, Caroline Daneault, Jean-Louis Vanoverschelde, Christine Des Rosiers, Louis Hue, Sandrine Horman, Christophe Beauloye, Luc Bertrand Metabolism and acetylation contribute to leucine-mediated inhibition of cardiac glucose uptake Am J Physiol Heart Circ Physiol, published online June 23, 2017. DOI: 10.1152/ajpheart.00738.2016
July 20, 2017
Are calcium alternans in the post-MI border zone more susceptible to the effects of sympathetic stimulation than in normal zone cardiomyocytes? In this podcast Consulting Editor Crystal Ripplinger uncovers the answer in her interview with lead author Jordi Heijman and content expert Thomas Hund about the recent work by Tomek et al. Heijman and co-authors explored sympathetic stimulation and its role in arrhythmogenesis by applying an innovative computational model to the canine post-MI border zone. Did Heijman and colleagues find that β-adrenergic stimulation suppressed alternans by one single mechanism or via multiple pathways? Did Heijman and co-authors also find that hyperinnervation in the border zone is actually anti-arrhythmic, by preventing alternans? Listen and find out.
Jakub Tomek, Blanca Rodriguez, Gil Bub, Jordi Heijman β-adrenergic receptor stimulation inhibits proarrhythmic alternans in post-infarction border zone cardiomyocytes: a computational analysis Am J Physiol Heart Circ Physiol, published online May 26, 2017. DOI: 10.1152/ajpheart.00094.2017