Ca2+, Trpm2 and Mitochondria

Is calcium entry into the heart via Trpm2 channels critical for maintaining cardiomyocyte bioenergetics and function? Listen as Associate Editor Ronglih Liao (Brigham and Women's Hospital and Harvard Medical School) interviews senior author Joseph Cheung (Temple University School of Medicine) and content expert Nazareno Paolocci (Johns Hopkins University School of Medicine) about the fascinating and comprehensive new study by Hoffman et al. By challenging conventional wisdom that calcium entry through Trpm2 channels worsens ischemia-reperfusion injury, Cheung and collaborators were surprised to discover the reverse—that by knocking out Trpm2 channels, ischemia-reperfusion injury was far worse than expected. Did Cheung and colleagues find that Trpm2 protects cardiomyocytes from ischemia-reperfusion dysfunction? Listen now.


Nicholas E. Hoffman, Barbara A. Miller, JuFang Wang, John W. Elrod, Sudasan Rajan, Erhe Gao, Jianliang Song, Xue-Qian Zhang, Iwona Hirschler-Laszkiewicz, Santhanam Shanmughapriya, Walter J. Koch, Arthur M. Feldman, Muniswamy Madesh, Joseph Y. Cheung Ca2+ entry via Trpm2 is essential for cardiac myocyte bioenergetics maintenance Am J Physiol Heart Circ Physiol, published March 15, 2015, doi: 10.1152/ajpheart.00720.2014.

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Caveolin-1 and Angiotensin Receptor Interaction in Obesity

What is the role of angiotensin receptor trafficking in small artery constriction, and what is its contribution to obesity-associated microvascular dysfunction? In this podcast Associate Editor Fabio Recchia (Temple University and Scuola Superiore S. Anna, Pisa) interviews lead author Zsolt Bagi (Georgia Regents University) and content expert Prasad Katakam (Tulane University School of Medicine) about the novel work by Czikora et al., which explores the hypothesis that the interaction between type 1 angiotensin II receptor and caveolin-1 is essential to prevent sustained angiotensin-II induced constriction in resistance arteries. Given the close association between obesity and hypertension, are there potential clinical applications for this work, with the goal to help restore normal regulatory function of caveolin-1 in obese human patients? Listen and learn.


Istvan Czikora, Attila Feher, Rudolf Lucas, David J. R. Fulton, Zsolt Bagi Caveolin-1 prevents sustained angiotensin II-induced resistance artery constriction and obesity-induced high blood pressure Am J Physiol Heart Circ Physiol, published March 1, 2015. DOI: 10.1152/ajpheart.00649.2014.

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Cardiac Mineralocorticoid Receptors Diastolic Dysfunction

What role does a “Western diet” –one largely centered around high fat and high fructose corn syrup intake—play in the metabolic syndrome of insulin resistance, diabetes, and obesity? Deputy Editor Dr. Merry Lindsey (University of Mississippi Medical Center) interviews first author Dr. Brian Bostick (University of Missouri) and content expert Dr. Nikolaos Frangogiannis (Albert Einstein College of Medicine) in this latest podcast exploring the unique bedside-to-bench work by Bostick and colleagues. Using the recent TOPCAT trial as a springboard, Bostick and co-authors examined whether spironolactone had any beneficial effects on mice with obesity and over-nutrition induced diastolic dysfunction. Listen as we explore how treatment with spironolactone affected M1 and M2 macrophages differently. With more than half of heart failure patients admitted to hospitals today suffering from diastolic dysfunction, does spironolactone have promising therapeutic applications related to obesity and cardiac function?


Brian Bostick, Javad Habibi, Vincent G. DeMarco, Guanghong Jia, Timothy L. Domeier, Michelle D. Lambert, Annayya R. Aroor, Ravi Nistala, Shawn B. Bender, Mona Garro, Melvin R. Hayden, Lixin Ma, Camila Manrique Acevedo, James R. Sowers Mineralocorticoid Receptor Blockade Prevents Western Diet-induced Diastolic Dysfunction in Female Mice Am J Physiol Heart Circ Physiol, published online March 7, 2015, doi: 10.1152/ajpheart.00898.2014.

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