Mitochondrial Flash: Novel Biomarker of Mitochondrial Respiration

What are mitochondria flash events, and are the flash coupled to the flow of electrons along the electron transport chain during mitochondrial respiration? In this podcast Associate Editor Ronglih Liao (Brigham and Women's Hospital and Harvard Medical School) interviews lead author Wang Wang (University of Washington) and content expert Hossein Ardehali (Northwestern University) about the study by Gong et al, which goes beyond Wang’s pioneering discovery of mitochondria flash to imaging flash and measuring mitochondria respiration. Might the imaging techniques used by Wang and co-authors lead to analysis of mitochondrial respiration in tissues other than the heart, such as skeletal muscle? While mitochondria flash can be used to measure reactive oxygen species (ROS) production inside the cell, can this innovative technique, in combination with pharmacological approaches, pinpoint the exact source of ROS production? Listen to find out.


Guohua Gong, Xiaoyun Liu, Huiliang Zhang, Shey-Shing Sheu, Wang Wang Mitochondrial flash as a novel biomarker of mitochondrial respiration in the heart Am J Physiol Heart Circ Physiol, published October 1, 2015, DOI: 10.1152/ajpheart.00462.2015.

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Clock Dysfunction Triggers Fibrotic Response in the Heart

What is the role of the circadian clock component Bmal1 in cardiac function? Deputy Editor Merry Lindsey (University of Mississippi Medical Center) interviews lead author Ganesh Halade (University of Alabama at Birmingham) and expert Amanda Le Blanc (University of Louisville) in this engaging podcast about the work by the Young and Halade laboratories, which found a “striking” result: cardiomyocyte specific Bmal1 deletion not only triggered the development of diastolic dysfunction, adverse extracellular matrix remodeling, and inflammation, but also drastically reduced the lifespan of mice compared to control litter mates. Do the Ingle et al results indicate that cardiomyocytes are an early, upstream regulator of aging in the heart? Listen and learn.


Kevin A. Ingle, Vasundhara Kain, Mehak Goel, Sumanth D. Prabhu, Martin E. Young, Ganesh V Halade Cardiomyocyte specific Bmal1 deletion in mice triggers diastolic dysfunction, extracellular matrix response and impaired resolution of inflammation Am J Physiol Heart Circ Physiol, published online October 2, 2015, DOI: 10.1152/ajpheart.00608.2015.

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Heart Failure Alters Synaptic Input in Cardiac Vagal Neurons

Is a reduction in parasympathetic activity the “canary in the coal mine” at the onset of many cardiovascular diseases, such as hypertension and heart failure? Listen as Associate Editor Kaushik Patel (University of Nebraska Medical Center) interviews lead author David Mendelowitz (George Washington University) and content expert Helio Salgado (University of São Paulo) about why Cauley et al set out to understand what changes cardiac vagal activity at the level of the brainstem using an aortic constriction model of heart failure. While much is known about alterations in sympathetic nerve activity, the knowledge of parasympathetic activity is still in its infancy. Could leveraging the diverse populations of neurons within the paraventricular nucleus of the hypothalamus provide a mechanism to alter the sympathetic-parasympathetic balance? Would stimulating parasympathetic activity, either at the level of the ganglia or brainstem, provide cardioprotective benefits in cardiovascular diseases, such as hypertension and heart failure? Listen to find out.


Edmund Cauley, Xin Wang, Jhansi Dyavanapalli, Ke Sun, Kara Garrott, Sarah Kuzmiak-Glancy, Matthew W Kay, David Mendelowitz Neurotransmission to Parasympathetic Cardiac Vagal Neurons in the Brainstem is Altered With Left Ventricular Hypertrophy Induced Heart Failure Am J Physiol Heart Circ Physiol, published September 14, 2015, DOI: 10.1152/ajpheart.00445.2015.

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CLIC4 Regulates Maturation of Cerebral Collaterals

What are collateral arterioles, and how can the number of such collaterals in the brain affect recovery from stroke? Listen as Guest Editor Akos Koller (New York Medical College) interviews first author Jennifer Lucitti (University of North Carolina at Chapel Hill) and content expert Mordecai Blaustein (University of Maryland Medical School) about this fascinating new study, which investigated the formation of collaterals both pre- and postnatal, as well as the role of chloride intracellular channel 4 (CLIC4) protein in collateral formation. Lucitti and colleagues found that there is a specific time when collaterals formed during embryogenesis, which can be very important later in life if larger arteries are blocked. At the molecular level, what exciting relationship did the authors find between vascular endothelial growth factor-A (VEGF-A) and CLIC 4 during collaterogenesis? Is prevention of collateral pruning and enhancement of collateral stabilization later in life a promising therapeutic target for stroke? Listen now.


Jennifer L. Lucitti, Natalie J. Tarte, James E. Faber Chloride intracellular channel 4 is required for maturation of the cerebral collateral circulation Am J Physiol Heart Circ Physiol, published October 1, 2015, DOI: 10.1152/ajpheart.00451.2015.

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