AJP-Heart and Circulatory Physiology Podcasts
Daylight Saving Time and Cardiovascular Risk

Daylight Saving Time and Cardiovascular Risk

August 2, 2022

Is it bad for our cardiovascular health to “spring forward” into Daylight Saving Time? On March 15, 2022, the U.S. Senate passed the Sunshine Protection Act, which aims to make Daylight Saving Time permanent and eliminate bi-annual seasonal clock changes in the spring and fall. In this episode, Consulting Editor Dr. Austin Robinson (Auburn University) interviews lead author and Associate Editor Dr. Jason Carter (Montana State University) and expert Dr. Josiane Broussard (Colorado State University) about a Perspective by Carter et al. which unpacks the negative impacts on overall cardiovascular health, as well as the increased risks of adverse cardiovascular events associated with changing our clocks between Standard Time and Daylight Saving Time. While the proposed Sunshine Protection Act legislation appears to offer a solution—instituting Daylight Saving Time as the permanent time – both the American Academy of Sleep Medicine and the Society for Research on Biological Rhythms argue that the healthier choice is Standard Time. Studies have shown that the shift to Daylight Saving Time results in increased incidence of myocardial infarction, stroke, and hospital admissions attributed to atrial fibrillation. In addition, the decrease in morning light with Daylight Saving Time has potential adverse effects on mental health, because morning sunshine plays a critical role in synchronizing our internal clocks to avoid circadian misalignment. Could shifting 30 minutes rather than 60 minutes be a reasonable compromise? Listen now to find out.

 

Jason R. Carter, Kristen L. Knutson, Babak Mokhlesi Taking to “heart” the proposed legislation for permanent daylight saving time Am J Physiol Heart Circ Physiol, published June 13, 2022. DOI: doi.org/10.1152/ajpheart.00218.2022

SRPK1 Eye Drops as a Treatment for Diabetic Retinopathy

SRPK1 Eye Drops as a Treatment for Diabetic Retinopathy

July 25, 2022

The eyes are the window to the soul, as the old saying goes, but are the eyes also the window to cardiovascular disease? Diabetic retinopathy is a common diabetic microvascular disease and a leading cause of blindness in diabetes patients worldwide. Defects in the blood-retinal barrier caused by increased production of vascular endothelial growth factor-A isoforms promote angiogenesis and permeability. Listen as Consulting Editor Dr. Shawn Bender (University of Missouri, Columbia) interviews first author Dr. Naseeb Malhi (City of Hope National Medical Center), senior author Dr. David Bates (University of Nottingham), and expert Dr. Jerome Breslin (University of South Florida) about the new study by Malhi et al, which investigated whether serine-arginine-rich protein kinase-1 (SRPK1) inhibition can attenuate the pathophysiology of diabetic retinopathy. The authors conducted a combination of mechanistic in vitro studies using human retinal pigment epithelial cells and studies in type 1 diabetic rats to investigate whether SRPK1 is activated in diabetes, and whether an SRPK1 inhibitor (SPHINX31) switches VEGF splicing in diabetic retinopathy to prevent increased vascular permeability into the retina. The novel intervention design of delivering the SRPK1 inhibitor via eyedrop in the authors’ diabetic rat model was used preventatively at the outset of the diabetes phenotype. Does this unique treatment modality offer promise for treating established diabetic retinopathy? Listen and learn.

 

Naseeb K. Malhi, Claire L. Allen, Elizabeth Stewart, Katherine L. Horton, Federica Riu, Jennifer Batson, Winfried Amoaku, Jonathan C. Morris, Kenton P. Arkill, David O. Bates Serine-arginine-rich protein kinase-1 inhibition for the treatment of diabetic retinopathy Am J Physiol Heart Circ Physiol, published May 10, 2022. DOI: 10.1152/ajpheart.00001.2022

Behind the Bench Episode 12

Behind the Bench Episode 12

July 6, 2022

This episode of Behind the Bench with AJP-Heart and Circ is full of connections. Returning co-host Dr. Charlotte Usselman is joined by her new co-host Dr. Tommy Martin. We first met Tommy when we interviewed him last year for Behind the Bench episode 10 as a trainee in the lab of AJP-Heart and Circ Associate Editor Dr. Jonathan Kirk. Jonathan was the original co-host of Behind the Bench along with Dr. Lisandra de Castro Brás. Speaking of Jonathan and Lis… big shout out to the original Behind the Bench co-hosts for their stellar insights and witty humor! Fast forward to the proverbial passing of the Behind the Bench microphone to Charlotte and Tommy and their wide-ranging interview with Dr. Jody Greaney, lead author of a new study interrogating vascular dysfunction as one mechanism, of the many potential mechanisms, linking major depressive disorder to CV disease risk. Greaney and co-authors investigated upstream mechanisms of vascular dysfunction and increased vascular superoxide by targeting inflammation with short-term salicylate treatment in a young adult population with major depressive disorder and found that this treatment did improve microvascular endothelium-dependent dilation. Listen as Jody discusses how she persevered with her small proof-of-concept study through finishing her post-doc, obtaining a faculty position, navigating the start-up her own lab, pandemic related interruptions to basic research, and peer reviewer comments that seemed daunting to overcome. Could depression, at its core, be characterized as an inflammatory disease? Are you at a critical career fork in the road and need some insight? Listen now.

 

Jody L. Greaney, Erika F. H. Saunders, Lacy M. Alexander Short-term salicylate treatment improves microvascular endothelium-dependent dilation in young adults with major depressive disorder
Am J Physiol Heart Circ Physiol
, published April 14, 2022. DOI: 10.1152/ajpheart.00643.2021

Vascular Function, Mortality and COVID-19

Vascular Function, Mortality and COVID-19

June 17, 2022

First, a thank you to frontline healthcare workers, clinical researchers, and one determined master’s student Michelle Cristina-Oliveira of the Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo for their bravery and dedication to science and medicine!
In this episode we bring you a conversation between Associate Editor Dr. Jason Carter (Montana State University), lead author Dr. Tiago Pecanha (Universidade de São Paulo, and Manchester Metropolitan University), and expert Dr. Paul Fadel (The University of Texas at Arlington). From June 2020 to May 2021 first author Michelle Cristina-Oliveira screened over 600 patients at the height of the COVID-19 pandemic in São Paulo, Brazil in order to enroll 211 COVID-19 patients within 72 hours of hospital admission. The authors sought to determine whether brachial artery flow-mediated dilation and carotid intima-media thickness measured upon hospital admission were associated with acute outcomes in hospitalized COVID-19 patients. Based on initial case reports, Cristina-Oliveira et al. felt that the endothelium could be an important target for SARS-CoV2. The authors hypothesized that measuring markers of endothelial function and atherosclerosis upon hospital admission could provide critically important information about potential risks of mortality, admission to ICU, and requirement for mechanical ventilation. Did the authors find that endothelial function and atherosclerosis were useful in predicting major clinical outcomes of COVID-19 patients? This study lends further insight into understanding the role of reduced flow mediated dilation in mediating the negative effects of COVID on cardiovascular health. Listen to find out why.

 

Michelle Cristina-Oliveira, Kamila Meireles, Saulo Gil, Fábio Cavalcante Assis, João Carlos Geber-Júnior, Samuel Katsuyuki Shinjo, Heraldo Possolo de Souza, Alfredo Nicodemos Cruz Santana, Paul A. Swinton, Luciano F. Drager, Bruno Gualano, Hamilton Roschel, and Tiago Peçanha Carotid intima-media thickness and flow-mediated dilation do not predict acute in-hospital outcomes in patients hospitalized with COVID-19 Am J Physiol Heart Circ Physiol, published April 22, 2022. DOI: 10.1152/ajpheart.00026.2022

Prenatal Dexamethasone Alters Female Cardiovascular Function

Prenatal Dexamethasone Alters Female Cardiovascular Function

June 6, 2022

How does in utero glucocorticoid administration impact autonomic control of the heart in adult offspring in a sex-dependent manner? In this episode, Associate Editor Dr. Crystal Ripplinger (University of California – Davis) interviews authors Dr. Taben Hale and Lakshmi Madhavpeddi (University of Arizona) along with expert Dr. Glen Pyle (University of Guelph) about the new work by Madhavpeddi et al. The authors administered dexamethasone to pregnant rats using a dose and timing that closely mimicked clinical application of dexamethasone administration to pregnant women at risk for preterm delivery to prevent respiratory distress in newborns. At baseline, the authors did not observe any differences between the prenatally-exposed offspring and controls. In response to an experimental stressor, however, the authors found that prenatal exposure to dexamethasone resulted in exaggerated blood pressure and heart rate only in adult female rats. Prenatally-exposed adult male rats did not exhibit any stress response changes in cardiovascular function. In addition, only the dexamethasone-exposed adult female offspring showed a reduction in the high frequency component of heart rate variability, indicating withdrawal of parasympathetic activity. What role does angiotensin II play in the altered autonomic response induced by prenatal dexamethasone exposure? Can we derive important potential clinical applications of this work related to the long-term impact on offspring from treatments administered during their mothers’ pregnancies? Listen now to find out.

 

L. Madhavpeddi, B. Hammond, D. L. Carbone, P. Kang, R. J Handa, T. M. Hale Impact of angiotensin II receptor antagonism on the sex-selective dysregulation of cardiovascular function induced by in utero dexamethasone exposure Am J Physiol Heart Circ Physiol, published March 17, 2022. DOI: 10.1152/ajpheart.00587.2021

The AJP-Heart and Circ Podcast Special Anniversary Episode #300

The AJP-Heart and Circ Podcast Special Anniversary Episode #300

June 2, 2022

Who knew that back in 2010, when previous Editor-in-Chief Dr. Bill Stanley said, “Podcasts! I don’t know anything about them, but I think we should do them!,” that we would still be producing The AJP-Heart and Circ Podcast 12 years and 299 episodes later?!  Since then we have talked with hundreds of authors, experts and editors around the world about the innovative and impactful research published in AJP-Heart and Circulatory Physiology. In this special anniversary episode #300, we turn the tables on our usual format. Executive Editor and podcast producer Kara Hansell Keehan interviews Editor-in-Chief Dr. Merry Lindsey (University of Nebraska Medical Center), Deputy Editor Dr. Zamaneh Kassiri (University of Alberta), and Associate Editors Dr. Keith Brunt (Dalhousie University), Dr. Jason Carter (Montana State University), Dr. Jonathan Kirk (Loyola University Chicago), Dr. Petra Kleinbongard (University of Duisburg-Essen Medical School), Dr. Amanda Jo LeBlanc (University of Louisville), and Dr. Crystal Ripplinger (University of California-Davis). Why should authors submit to AJP-Heart and Circ? What advice do the AJP-Heart and Circ editors have for early career researchers? And finally, what do the editors have to say about the value of The AJP-Heart and Circ Podcast for our listeners?  There is only one way to find out. Listen now.

GLS1 Inhibition Improves Cardiac Remodeling — Japanese Language Version

GLS1 Inhibition Improves Cardiac Remodeling — Japanese Language Version

April 28, 2022

Are failing hearts addicted to glutamine? In this special episode of The AJP-Heart and Circ Podcast, we bring you a conversation in both Japanese and English with Editorial Board member Dr. Junichi Sadoshima (Rutgers University-New Jersey Medical School), Consulting Editor Dr. Jun Yoshioka (City University of New York School of Medicine), and corresponding author Dr. Manabu Nagao (Kobe University Graduate School of Medicine) about the new study by Yoshikawa et al. that explores the interaction between metabolism and pathophysiological cardiac hypertrophy. It is well known that the heart uses various substrates to produce ATP during cardiac hypertrophy. Earlier observations about how cancer cells rapidly consume glutamine during the tumor growth phase led the authors to interrogate the role of glutamine metabolism in cardiac hypertrophy. Nagao and co-authors show that glutaminase is upregulated during cardiac hypertrophy, and that suppression of glutaminase 1 (GLS1) attenuates cardiac hypertrophy. GLS1-mediated glutaminolysis contributes to maladaptive cardiac remodeling by increasing anabolic reactions for hypertrophy and proliferation. Glutamine metabolism is essential for cardiomyocytes. Interestingly, glutaminolysis is activated much faster than glucolysis in response to acute stress. Yoshikawa et al. show that a counter-clockwise shift of the tricarboxylic acid cycle contributes to cardiac remodeling. This study is a game-changer. Listen to learn why.

 

Sachiko Yoshikawa, Manabu Nagao, Ryuji Toh, Masakazu Shinohara, Takuya Iino, Yasuhiro Irino, Makoto Nishimori, Hidekazu Tanaka, Seimi Satomi-Kobayashi, Tatsuro Ishida, and Ken-Ichi Hirata Inhibition of glutaminase 1-mediated glutaminolysis improves pathological cardiac remodeling Am J Physiol Heart Circ Physiol, published March 30, 2022. DOI: 10.1152/ajpheart.00692.2021

GLS1 Inhibition Improves Cardiac Remodeling — English Language Version

GLS1 Inhibition Improves Cardiac Remodeling — English Language Version

April 28, 2022

Are failing hearts addicted to glutamine? In this special episode of The AJP-Heart and Circ Podcast, we bring you a conversation in both Japanese and English with Editorial Board member Dr. Junichi Sadoshima (Rutgers University-New Jersey Medical School), Consulting Editor Dr. Jun Yoshioka (City University of New York School of Medicine), and corresponding author Dr. Manabu Nagao (Kobe University Graduate School of Medicine) about the new study by Yoshikawa et al. that explores the interaction between metabolism and pathophysiological cardiac hypertrophy. It is well known that the heart uses various substrates to produce ATP during cardiac hypertrophy. Earlier observations about how cancer cells rapidly consume glutamine during the tumor growth phase led the authors to interrogate the role of glutamine metabolism in cardiac hypertrophy. Nagao and co-authors show that glutaminase is upregulated during cardiac hypertrophy, and that suppression of glutaminase 1 (GLS1) attenuates cardiac hypertrophy. GLS1-mediated glutaminolysis contributes to maladaptive cardiac remodeling by increasing anabolic reactions for hypertrophy and proliferation. Glutamine metabolism is essential for cardiomyocytes. Interestingly, glutaminolysis is activated much faster than glucolysis in response to acute stress. Yoshikawa et al. show that a counter-clockwise shift of the tricarboxylic acid cycle contributes to cardiac remodeling. This study is a game-changer. Listen to learn why.

 

Sachiko Yoshikawa, Manabu Nagao, Ryuji Toh, Masakazu Shinohara, Takuya Iino, Yasuhiro Irino, Makoto Nishimori, Hidekazu Tanaka, Seimi Satomi-Kobayashi, Tatsuro Ishida, and Ken-Ichi Hirata Inhibition of glutaminase 1-mediated glutaminolysis improves pathological cardiac remodeling Am J Physiol Heart Circ Physiol, published March 30, 2022. DOI: 10.1152/ajpheart.00692.2021

Beta1-Adrenergic Receptor Cleavage by Trypsin

Beta1-Adrenergic Receptor Cleavage by Trypsin

April 25, 2022

Impactful findings with reverberating consequences – this is what AJP-Heart and Circ Rapid Reports are here for. Listen as Associate Editor Dr. Jonathan Kirk (Loyola University Chicago Stritch School of Medicine) interviews lead author Dr. Susan Steinberg (Columbia University) and expert Dr. Michael Kapiloff (Stanford University) about this novel work by Zhu and Steinberg. More than 20 years ago, Steinberg and collaborators used immunoblot analysis to implicate compartmentalization as a mechanism that imparts beta-adrenergic receptor subtype signaling specificity. Of note, these studies also provided the unexpected observation that the beta1-adrenergic receptor subtype accumulates as both full-length and N-terminally truncated species; in contrast, beta2-adrenergic receptors are expressed exclusively as a single full-length species. The Steinberg laboratory went on to identify the molecular mechanisms that control the maturational processing of the full-length receptor to an N-terminally truncated form (including the role of a member of the matrix metalloproteinase family of enzymes) and the functional importance of this finding. They showed that full-length and N-terminally truncated beta1-adenergic receptors differ in their signaling phenotype; the N-terminally truncated beta1-adenergic receptor plays a unique role to constitutively activate an AKT signaling pathway that is cardioprotective.

 

This Rapid Report expands upon the previous studies by showing that the beta1-adrenergic receptor is also cleaved by trypsin, an enzyme used in protocols to isolate cardiomyocytes from ventricular tissue. This finding suggests that studies on cardiomyocytes isolated in this manner should be interpreted with caution. In the broader context, the cleavage mechanism that regulates beta1-adrenergic receptor signaling uncovered by Zhu and Steinberg has important clinical implications given the fact that beta-adrenergic receptors are first-line targets for heart failure (with beta blockers one of the most prescribed medications). The podcast discusses several questions. Are beta1-adrenergic receptors also cleaved (and hence catecholamine responsiveness also altered) by functionally relevant inflammatory proteases in the setting of cardiac injury or myocarditis? Do the full-length and truncated forms of the beta1-adrenergic receptor play distinct roles in the evolution of heart failure? This research clearly is a springboard for future studies. Listen and find out why.

 

Jing Zhu and Susan F. Steinberg Trypsin cleavage of the beta1-adrenergic receptor Am J Physiol Heart Circ Physiol, published March 1, 2022. DOI: 10.1152/ajpheart.00005.2022

Murine MI Sizing with 2D and 4D Echocardiography

Murine MI Sizing with 2D and 4D Echocardiography

April 6, 2022

While echocardiography is commonly used to assess cardiac structure and function in mouse models of heart disease, can this non-invasive technique also be used to accurately measure infarct size? Listen as Deputy Editor Dr. Zamaneh Kassiri (University of Alberta) interviews co-authors Dr. Erin Mulvihill (University of Ottawa) and Dr. Craig Goergen (Purdue University), along with content expert Dr. Daniele Panetta (Institute of Clinical Physiology CNR - Pisa). Dann et al. measured and monitored infarct size by comparing and contrasting 2-D echo imaging results with 4-D echo imaging results in a myocardial infarction mouse model. 4-D ultrasound imaging allowed the authors to measure the entire volume of the left ventricle throughout the cardiac cycle, as well as analyze the progression of asymmetric ventricular remodeling. In addition, this work illustrates how authors from two different academic institutions found a novel way to collaborate during the COVID-19 pandemic and ensuing international travel restrictions. The study by Dann et al. provides a unique visualization of the infarct in 3-D, which then allowed for volumetric analysis to use contouring of the heart to produce dynamic strain maps. Listen as we discuss how the innovative imaging modalities utilized by Dann et al. allow researchers to focus on animal specific differences as well as the inclusion of both female and male animals for robust rigor and reproducibility.

 

Melissa M. Dann, Sydney Q. Clark, Natasha A. Trzaskalski, Conner C. Earl, Luke E. Schepers, Serena M. Pulente, Ebonee N. Lennord, Karthik Annamalai, Joseph M. Gruber, Abigail D. Cox, Ilka Lorenzen-Schmidt, Richard Seymour, Kyoung-Han Kim, Craig J. Goergen, and Erin E. Mulvihill Quantification of murine myocardial infarct size using 2-D and 4-D high-frequency ultrasound  
Am J Physiol Heart Circ Physiol, published February 8, 2022. DOI: doi.org/10.1152/ajpheart.00476.2021

Podbean App

Play this podcast on Podbean App