AJP - Heart and Circulatory Physiology

The obesity epidemic in the United States shows no signs of abating, which is why our latest podcast is particularly insightful. Associate Editor Nancy Kanagy talks with author Lusha Xiang (University of Mississippi) and leading expert Jeff Frisbee (West Virginia University) about the study by Xiang and colleagues, which suggests the mechanism behind the poor prognosis for obese trauma victims and provides insight into a new therapeutic intervention to improve recovery of obese victims of traumatic injury.

Lusha Xiang, Silu Lu, William Fuller, Arun Aneja, George V Russell, Louis B Jones, and Robert L. Hester. Impaired blood pressure recovery to hemorrhage in obese Zucker rats with orthopedic trauma. Am J Physiol Heart Circ Physiol, published ahead of print October 14, 2011, doi: 10.1152/ajpheart.00439.2011.

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A well-known problem for heart failure patients is the inability, or markedly decreased ability, to exercise. When even low levels of daily activity are impaired, the quality of life for heart failure patients suffers considerably. The mechanisms for exercise intolerance are very complicated and extend far beyond impaired cardiac performance. Listen in as Associate Editor Irving Zucker, senior author David Poole (Kansas State University) and leading expert Peter Wagner (University of California, San Diego) discuss the new Review article by Poole and colleagues, which tackles the mechanisms of muscle dysfunction in heart failure at the oxygen transport and microcirculatory levels.

David C. Poole, Daniel M. Hirai, Steven W. Copp, and Timothy I. Musch. Muscle Oxygen Transport and Utilization in Heart Failure: Implications for Exercise (In)tolerance Am J Physiol Heart Circ Physiol, published ahead of print November 18, 2011, doi:10.1152/ajpheart.00943.2011.

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What are the parameters which modulate conduction under normal and disease conditions in the heart? This age-old debate has pitted two distinct schools of thought against each other—ephaptic conduction vs. gap junctions. Can changes in interstitial volume by pharmacological means dramatically change conduction velocity? In our latest podcast on the article by Veeraraghavan et al, Associate Editor Igor Efimov, leading expert Craig Henriquez (Duke University) and senior author Steven Poelzing (University of Utah) wade into the debate.

Rengasayee Veeraraghavan, Mohamed E. Salama, and Steven Poelzing. Interstitial volume modulates the conduction velocity-gap junction relationship. Am J Physiol Heart Circ Physiol, published ahead of print October 21, 2011, doi: 10.1152/ajpheart.00868.2011.

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Our latest podcast focuses on mitochondrial dynamics, as senior author Ken Walsh (Boston University) and expert Elizabeth “Tish” Murphy (NHLBI) join Consulting Editor Michael Wolin to discuss the recent study by Papanicolau et al, showing surprising effects of cardiac deletion of the key mitochondrial membrane protein mitofusin-1. Listen in as we uncover the unexpected impact of mitofusin-1 and mitofusin-2 on mitochondrial size and resistance to stress.

Kyriakos N. Papanicolaou, Gladys A. Ngoh, Errine R Dabkowski, Kelly A O'Connell, Rogerio F. Ribeiro, William C. Stanley, and Kenneth Walsh. Cardiomyocyte deletion of mitofusin-1 leads to mitochondrial fragmentation and improves tolerance to ROS-induced mitochondrial dysfunction and cell death. Am J Physiol Heart Circ Physiol, published ahead of print October 28, 2011, doi: 10.1152/ajpheart.00833.2011.

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Post-translational modification through acetylation by the NAD+-dependent deacetylase sirtuin-3, or SIRT3, has recently emerged as a key player in regulating mitochondrial function. What is SIRT3 doing in cardiac mitochondria? How does it impact cardiac physiology and pathophysiology? Listen as Editor in Chief William Stanley and Associate Editor Junichi Sadoshima talk with the author Michael Sack (National Heart, Lung and Blood Institute, NIH) about his just-published Review article which tackles these very questions.

Michael N. Sack. Emerging characterization of the role of SIRT3 mediated mitochondrial protein deacetylation in the heart. Am J Physiol Heart Circ Physiol, published ahead of print October 7, 2011, doi:10.1152/ajpheart.00199.2011.

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The discovery of induced pluripotent stem (iPS) cells has allowed researchers to generate human cardiomyocytes from patients. Why is this important? Human iPS cells are useful for studying normal and diseased human cardiomyocytes and for discovering new drug therapies to treat cardiovascular disease. Until now, methods for generating cardiomyocytes from human iPS or ES cells were inconsistent and often unreliable. The recent article by Ma et al presents a new method to obtain a large quantity of cultured cardiac myocytes using embryoid body formation and blasticidin selection techniques resulting in more than 98% purity from human iPS cell lines. Associate Editor Junichi Sadoshima talks with authors Craig January (University of Wisconsin – Madison) and Brad Swanson (Cellular Dynamics International), along with leading expert Diego Fraidenraich (University of Medicine and Dentistry, New Jersey), about this groundbreaking research and its many potential applications.

Junyi Ma, Liang Guo, Steve J Fiene, Blake D Anson, James A Thomson, Timothy J. Kamp, Kyle L Kolaja, Bradley J Swanson, and Craig T. January. High Purity Human Induced Pluripotent Stem Cell (hiPSC) Derived Cardiomyocytes: Electrophysiological Properties of Action Potentials and Ionic Currents. Am J Physiol Heart Circ Physiol, published ahead of print September 2, 2011, doi:10.1152/ajpheart.00694.2011.

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It almost goes without saying that human beings are genetically diverse and that diseases develop differently, and at different rates, across various racial groups in the human population. Case in point: African Americans are predisposed to developing far deadlier forms of hypertension earlier in life than other racial group counterparts. Associate Editor Irving Zucker talks with lead author David Keller (University of Texas Arlington) and expert Peter Raven (University of North Texas Health Science Center) about the work of Holwerda et al, which studied the possibility of the baroreflex contributing to the development of hypertension in African American males.

Seth W. Holwerda, Diana Fulton, Wendy L. Eubank, and David M. Keller. Carotid Baroreflex Responsiveness is Impaired in Normotensive African American Men. Am J Physiol Heart Circ Physiol, October 2011 301:H1639-H1645; published ahead of print August 12, 2011, doi:10.1152/ajpheart.00604.2011.

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We know that the endothelial surface is coated with glycocalyx. But why should we be concerned about the effects of shedding the glycocalyx on microvascular hemodynamics? Editor in Chief William C. Stanley talks with senior author Herbert Lipowsky (Pennsylvania State University) and leading expert Jos A. Spaan (University of Amsterdam) about the unique model presented in the article by Lipowsky et al that mimics aspects of acute vascular inflammation and investigates how shedding of the glycocalyx impacts many pathologies including diabetes.

Herbert H. Lipowsky, Lujia Gao, and Anne Lescanic. Shedding of the Endothelial Glycocalyx in Arterioles, Capillaries and Venules and its Effect on Capillary Hemodynamics During Inflammation. Am J Physiol Heart Circ Physiol, published ahead of print September 16, 2011, doi:10.1152/ajpheart.00803.2011.

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Pulmonary hypertension affects millions of patients with increasing prevalence each year, and clinical treatments are still in their infancy. In our latest podcast, Associate Editor Leon de Windt talks with senior author Sebastien Bonnet (Universite Laval) and leading expert Laura Gonzalez Bosc (University of New Mexico) about the article by Paulin et al, which reports the first demonstration of DHEA blocking two major transcription factors—STAT3 and NFAT. Is DHEA, a commercially available natural steroid hormone and antioxidant, the newest entry point for pharmacological intervention and treatment of pulmonary hypertension? Listen in and find out.

Roxane Paulin, Jolyane Meloche, Maria Helena Jacob, Malik Bisserier, Audrey Courboulin, and Sebastien Bonnet. Dehydroepiandrosterone inhibits the Src/STAT3 constitutive activation in pulmonary arterial hypertension. Am J Physiol Heart Circ Physiol, published ahead of print September 2, 2011, doi:10.1152/ajpheart.00654.2011.

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In our latest podcast we explore the connections between the sarcoplasmic reticulum and the mitochondria within calcium regulation during signaling contractile function and regulation of mitochondrial metabolism. Associate Editor Gary Lopaschuk interviews senior author Gyorgy Csordas (Thomas Jefferson University) and leading expert Pal Pacher (National Institutes of Health), seeking to explore a central question in the work by Garcia-Perez et al—how are the SR and the mitochondria communicating with each other?

Cecilia Garcia-Perez, Timothy G. Schneider, Gyorgy Hajnoczky, and Gyorgy Csordas. Alignment of sarcoplasmic reticulum-mitochondrial junctions with mitochondrial contact points. Am J Physiol Heart Circ Physiol, published online ahead of print August 19, 2011, doi:10.1152/ajpheart.00397.2011.

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