About Us

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The Cincinnati Early-Career Cardiovascular Researchers (ECVR) Network is a trainee-led joint initiative between the University of Cincinnati (UC) and Cincinnati Children’s Hospital (CCHMC), dedicated to supporting the career development and training of students, postdoctoral fellows, and early stage investigators working in all areas of cardiovascular science. The Cincinnati ECVR seeks to bring together all members of the UC and CCHMC cardiovascular research community and foster collaborative interdisciplinary research, networking, and outreach.

Vision: To be a unique and comprehensive resource for early career cardiovascular scientists, helping them to develop the skills and connections they will need to become the next generation of leaders in cardiovascular research.

Mission: To promote collaborative interdisciplinary science, networking, career development, and community outreach opportunities among all UC and CCHMC cardiovascular researchers, by providing:

Annual symposia, networking events, and social outings that bring together early career researchers, members of the UC and CCHMC faculty, and local or national thought leaders in cardiovascular science.
Recurring data exchange and informal mentoring sessions for graduate students and junior researchers, led by senior postdoctoral researchers and early career faculty.
Ongoing partnerships with the local chapter of the American Heart Association, the University of Cincinnati Research Institute, the Heart Institute at Cincinnati Children’s, and the Heart, Lung and Vascular Institute of the University of Cincinnati.

ECVR Organizing Committee

**Stephanie L Kidder Bowers, Ph.D.; ECVR President**
Stephanie is currently a Postdoctoral Fellow in the Molkentin lab at the Heart Institute at Cincinnati Children’s Hospital Medical Center. Her current studies seek to determine molecular mechanisms that drive the progression of fibrosis and organ failure. In particular, Stephanie is interested in exploring how injury alters both beneficial and detrimental communication between cells and their surrounding tissue matrix. Her overall goal is to help advance our understanding of how different organ systems affect one another during both homeostasis and disease pathophysiology.

Malina J Ivey, Ph.D.; ECVR Vice President, Career Development Chair, *President Elect*
Malina is currently a Postdoctoral Fellow in the laboratory of Onur Kanisicak in the Department of Pathology and Laboratory Medicine at the University of Cincinnati. Her current research seeks to determine molecular mechanisms that drive the progression of fibrosis. The aim of these studies is to identify targets to halt fibrogenesis and eventual regeneration of damaged cardiac and skeletal muscle.

**Tanya Baldwin, Ph.D.; ECVR Secretary, Outreach Chair**
Tanya is a Research Fellow in the Department of Molecular Cardiovascular Biology at Cincinnati Children’s Hospital Medical Center with Jeff Molkentin. Her current research focuses on understanding the molecular pathways dependent on protein palmitoylation. The aim of these studies is to uncover the role of palmitoylation enzymes in in cardiac physiology and pathology. Her overall goal is to understand how post-translational modifications and protein-protein interactions drive cardiovascular signaling.

**Kelly Grimes, Ph.D; ECVR Social Media and Communications Chair**
Kelly is a Postdoctoral Fellow in the laboratory of Jeff Molkentin in the Department of Molecular Cardiovascular Biology at Cincinnati Children’s Hospital Medical Center. Her research delves into the molecular pathways that control how cardiomyocytes grow preferentially in one dimension or another, with a particular focus on cytoskeletal proteins. Elucidating how these proteins feed into the cardiomyocyte directional growth response will hopefully lead to a better understanding of hypertrophic and dilated cardiomyopathies, diseases that feature the pathological growth of cardiomyocytes in different directions.

**Shannon Jones; ECVR Graduate Student Liaison**
Shannon is a graduate student in the Department of Pathology and Laboratory Medicine at the University of Cincinnati's College of Medicine. In the laboratory of Onur Kanisicak, her research focuses on cardiac fibroblast-mediated extracellular matrix remodeling that occurs during cardiovascular disease with a specific interest in periostin, a protein expressed by activated fibroblasts. Her dissertation seeks to investigate the role of periostin in the maturation and activation of cardiac fibroblasts in order to better understand the mechanisms of cardiac fibrosis.

**Jose P. Guirao Abad, Ph.D.; ECVR Treasurer**
Jose is a Postdoctoral Fellow in the laboratories of Onur Kanisicak and David S. Askew in the Department of Pathology and Laboratory Medicine at the University of Cincinnati. His research seeks to unveil the role of pulmonary and cardiac fibroblasts in response to and clearance of airborne pathogens such as *Aspergillus fumigatus*. The main goal of his project is to improve our understanding of the host’s response to life-threatening infections. This research could impact future therapeutic strategies to improve the outcome of disease.

ECVR Faculty Advisory Committee

**Evangelia (Litsa) G. Kranias. Ph.D, FAHA, FISHR**
Hanna Professor and Director of Cardiovascular Biology; Distinguished Research Professor; Co-Director Cardiovascular Center of Excellence; Professor, Department of Pharmacology & Systems Physiology, University of Cincinnati
**Dr. Kranias’s** research program has focused on the role of calcium (Ca)-handling and Ca-signaling in regulation of myocardial function and survival in health and disease. The Kranias lab has provided fundamental insights into the mechanisms underlying impaired regulation of sarcoplasmic reticulum Ca-cycling in cardiac diseases, revealing new therapeutic modalities. Extension of these findings to the clinical arena, identified human variants in the key Ca-cycling genes that may serve as potential prognostic or diagnostic markers for heart failure and arrhythmia development.

**Katherine Yutzey, Ph.D.**
Professor of Pediatrics, Division of Molecular Cardiovascular Biology, Cincinnati Children’s Hospital
**Dr. Yutzey’s** lab focuses on the examination and manipulation of the molecular regulatory mechanisms of heart development and disease. The current main research areas of the lab are to further understand regulatory hierarchies that control 1. heart valve development, 2. cardiac fibroblast and extracellular matrix differentiation, and 3. cardiomyocyte maturation and proliferation in the large mammal. A goal of our research is to elucidate mechanisms of cardiovascular disease by combining studies investigating the regulatory pathways controlling normal cardiac development in animal models with analysis of the molecular progression of disease in pediatric and adult human tissue specimens.

**Onur Kanisicak, Ph.D.**
Assistant Professor, Department of Pathology and Laboratory Medicine, University of Cincinnati
**Dr. Kanisicak’s** research program focuses on the examination and manipulation of various cellular compartments within the cardiovascular system with an overall goal to identify novel therapeutic targets to prevent fibrosis and to promote cardiac wound healing. Towards these efforts, current projects in the Kanisicak lab employ in vivo genetic interrogation methods to determine the lineage plasticity and role of cardiac interstitial cells involved in fibrogenesis, as well as efforts to promote cardiomyocyte survival and enhance cardiac protection.

**Michael Tranter, Ph.D.**
Associate Professor, Department of Internal Medicine, Cardiovascular Research Center, University of Cincinnati
**Dr. Tranter’s** research program seeks to increase our understanding of the molecular mechanisms that drive cardiometabolic diseases. Ongoing projects in the lab are focused on post-transcriptional gene regulation by the RNA binding protein Human antigen R (HuR) in the setting of (1) the pathological progression of left ventricular hypertrophy and cardiac fibrosis leading to heart failure, (2) mechanisms of thermogenic metabolism in brown adipocytes, and (3) adipose tissue-mediated endocrine effects on cardiac physiology.
The lab was the first to show that HuR promotes cardiomyocyte hypertrophy following its cytoplasmic translocation induced downstream of p38 MAP kinase signaling and that cardiac-specific deletion or pharmacological inhibition of HuR preserves cardiac function while decreasing pathological ventricular remodeling and cardiac fibrosis following transverse aortic constriction (TAC), a model of hypertension-induced pathological cardiac hypertrophy. More recently, we have shown that adipocyte-specific HuR-deficient mice have impaired thermogenic activity of brown adipose tissue and demonstrated that adipocyte-specific deletion of HuR is sufficient to induce spontaneous cardiac hypertrophy and fibrosis in mice, suggesting these HuR-dependent pathways as novel mediators of adipose-myocardial endocrine signaling.

**Steve Standage, M.D.**
Assistant Professor, Department of Pediatrics, University of Cincinnati Attending Physician, Division of Critical Care Medicine, Cincinnati Children’s Hospital
The **Standage** lab investigates the molecular underpinnings of organ system failure in sepsis with a goal to elucidate targetable mechanisms with therapeutic potential. The laboratory currently focuses on understanding and manipulating metabolic and functional changes in the heart in sepsis, and has recently identified the peroxisome proliferator-activated receptor-α (PPARα), a nuclear hormone receptor transcription factor that regulates inflammation and lipid metabolism, as a key regulator of acute cardiac functional recovery and enhanced fatty acid metabolism during acute sepsis. Dr. Standage is also a faculty member of the CCHMC Critical Care Fellowship Program and an Attending Physician in the Cincinnati Children’s Hospital Pediatric Intensive Care Unit (PICU).

**Catherine (Cat) Makarewich, Ph.D.**
Assistant Professor, Division of Molecular Cardiovascular Biology, Heart Institute at Cincinnati Children’s Hospital
The **Makarewich** lab focuses on understanding the molecular mechanisms that underlie the pathophysiology of cardiovascular disease and skeletal muscle disorders. We use a combination of in vitro and in vivo methods to study the regulatory proteins that control the development, growth and function of cardiac and skeletal muscle in both health and disease. Recently, the cellular proteome has expanded to include a novel class of small proteins called microproteins, or micropeptides. These microproteins are translated from small open reading frames to generate proteins that are 100 amino acids or smaller. My research has been at the forefront of this evolving field of microprotein discovery and characterization. Our team has found that these microproteins play crucial roles in many essential biological processes including muscle contraction, metabolism and the maintenance of cellular calcium homeostasis. Our long-term objective is to use this information to generate new targeted therapies to prevent and treat heart disease and skeletal muscle disorders.

Mattia Quattrocelli, Ph.D.

Assistant Professor, Division of Molecular Cardiovascular Biology, Heart Institute at Cincinnati Children’s Hospital

The Quattrocelli Lab investigates molecular mechanisms and translatable biomarkers in dysfunction and rescue of striated muscles. The lab aims at combining genetics, epigenetics, and metabolism to garner a deeper understanding of muscle physiology and pharmacology. An important focus of the lab centers on “precision dosing” for glucocorticoid steroids in heart and muscle regulation. We are currently investigating how repetitive versus pulsatile regimens of these drugs remodel energy production and performance in several contexts of disease, including obesity, unhealthy aging, and heart failure. Moreover, we are leveraging the newly-discovered pharmacological mechanisms to expand the concept of precision dosing for these drugs to “chrono-pharmacology”. The overarching goal of the lab is to advance mechanistic understanding and applicable pharmacology to improve the health of heart and muscle.

**Chen Gao, Ph.D.**
Assistant Professor, Department of Pharmacology and Systems Physiology, College of Medicine, University of Cincinnati
The **Gao** Lab is focused on uncovering novel molecular mechanisms for the pathogenesis of cardiac diseases, including cardiac hypertrophy, remodeling, and dysfunction. The lab utilizes state-of-the-art molecular, genomic, and genetic tools to discover and interrogate key molecules involved in the understudied post-transcriptional processes in RNA metabolism in cardiac tissues under physiological and pathological states. Ultimately, the lab aims to develop novel therapeutic and diagnostic strategies for heart failure and cardiometabolic diseases.

**Konstantinos Drosatos, MSc, PhD, FAHA**
Ohio Eminent Scholar & Professor, Department of Pharmacology and Systems Physiology, College of Medicine, University of Cincinnati
Research in the **Drosatos** Lab focuses on signaling mechanisms that link cardiomyopathy in diabetes, sepsis and ischemia with altered myocardial and systemic metabolism. Their work has identified the transcriptional factor KLF5 as a regulator of cardiac fatty acid metabolism in diabetes, as well as a central cause for diabetic cardiomyopathy and ischemic heart failure. In addition, the Drosatos Lab study sepsis. Particularly, their work has signified the role of cardiac metabolism impairment, such as lower cardiac fatty acid oxidation and mitochondrial dysfunction, in the pathophysiology of septic cardiomyopathy. The Lab has been continuously funded by the NIH, the American Heart Association and other foundations.
Konstantinos Drosatos has extensive experience in promoting development of early career investigators. Besides being the recipient of the 2014 Outstanding Early Career Investigator Award of the American Heart Association-Basic Cardiovascular Sciences Council and the 2017 Early Research Investigator Award of the Medical School at Temple University, he is the founder of an annual international summer school for medical and biosciences students that has been running successfully for 10 years. He was also elected chair-elect of the Mid-Career Committee of the International Society for Heart Research and has served in the Early Career Committee of the Basic Cardiovascular Sciences Council of the American Heart Association.

Past Committee Members

**Sakthivel Sadayappan, Ph.D., M.B.A.; ECVR Co-Founder**
Professor, Department of Internal Medicine; Division of Cardiovascular Health and Disease, University of Cincinnati
Director of Heart Branch of the UC Heart, Lung and Vascular Institute
**Dr. Sadayappan** is a founding member of the ECVR and a Professor in the University of Cincinnati Heart, Lung and Vascular Institute. The Sadayappan lab is focused on elucidating the causes of muscle-specific diseases at the molecular level as well as identifying therapeutic targets that will lead to the development of effective cures for cardiac and skeletal muscle disease. Visit the Sadayappan Lab website to learn more.

**Ronald J Vagnozzi, Ph.D.; ECVR Co-Founder**
Ron is a founding member of the ECVR and served as ECVR President from 2016-2020. He is currently an Assistant Professor of Medicine in the Division of Cardiology, Gates Center for Regenerative Medicine, and Consortium for Fibrosis Research and Translation at the University of Colorado Anschutz Medical Campus. His lab studies cellular mechanisms of injury and stress responses in the heart, particularly the innate immune system and how inflammation impacts wound healing, fibrosis, and tissue remodeling.

McNamaraJames white coat.jpeg — **James W McNamara, Ph.D; ECVR Co-Founder**
James is currently a Research Officer at the Murdoch Children’s Research Institute in Melbourne, Australia. James was a founding member of the ECVR and served as Vice-President from 2016-2020, during his time as a Postdoctoral Fellow in the Sadayappan lab at the University of Cincinnati. His career is focused on defining novel myofilament-based mechanisms that contribute to striated muscle function. Currently, James is exploring the regulation of cardiac and skeletal muscles by the accessory protein, myosin binding protein-C, a potent modulator of contractility. James’ long-term goal is to uncover novel sarcomeric targets that can be therapeutically manipulated to modify muscle function.

**Mohit Kumar, Ph.D** was a Postdoctoral Fellow with Dr. Evangelia (Litsa) Kranias and Sakthivel Sadayappan at the University of Cincinnati. Mohit’s Ph.D. studies were focused on determining the role of cardiac myosin binding protein-C (cMyBP-C) phosphorylation in calcium handling in the heart. He has expertise in biophysical techniques measuring contractility at the sarcomere, muscle, and cardiac level. Mohit’s postdoctoral projects involve defining abnormal calcium handling with contractile dysfunction and activation of immune and inflammatory response post-myocardial infarction using both in vitro and in vivo models.

**Luis Hortells, DVM, Ph.D** was a Postdoctoral Fellow in Katherine Yutzey’s laboratory within the Heart Institute at Cincinnati Children’s Hospital. Luis focused on the role of cardiac fibroblast and the extracellular matrix in the postnatal heart maturation. He is currently studying the relevance of different types of fibroblast in the loss of myocardial regenerative capacity. His overall goal is to understand why the heart stops self-repairing, and in doing so, to try and find new pharmacological targets to treat heart disease.

Emma pic.jpg — **Emma J Agnew, CSci, MIFST** is a Scientific Advisor in the division of Food Protection Science and Surveillance for the Scottish Government. Prior to this, Emma was a Postdoctoral Fellow in the Molecular Cardiovascular Biology department at the Heart Institute of Cincinnati Children’s Hospital Medical Center. Her research focused on improving outcomes in patients with congenital heart defects through studying the ability of the large mammalian heart to regenerate and repair itself in the early stages post-birth.

**Michael J Bround, Ph.D** is a Postdoctoral Fellow in in the Division of Molecular Cardiovascular Biology and the Heart Institute at Cincinnati Children's Hospital. His research focuses on mitochondrial calcium signaling in cardiac and skeletal myocytes and how this process influences energy metabolism and cell death. His goal is to leverage a better understanding of mitochondrial calcium dynamics as a potential therapeutic axis to reduce necrotic cell death, especially following cardiac ischemia or myocardial infarction. Michael served as ECVR Secretary until 2020, and also designed the ECVR website.

**Hannah Russell, Ph.D.** was a Graduate Student in Phil Owens’ laboratory within the Heart, Lung and Vascular Institute at the University of Cincinnati’s College of Medicine. Hannah is interested in coagulation proteins and their wide effects through human physiology. The Owens Lab focuses in atherosclerosis and abdominal aortic aneurysm (AAA) with emphasis in coagulation proteins and platelet activity. Hannah’s dissertation project studies the role of fibrinogen in AAA pathogenesis.

**Lisa Green, Ph.D.** was a Graduate Student in Michael Tranter’s laboratory within the Heart Institute at the University of Cincinnati’s College of Medicine. Lisa is interested in the changes in gene expression throughout the progression of heart failure. The Tranter Lab has shown that HuR, an RNA binding protein, may play a role in the upregulation of pathological genes networks in the failing heart. Lisa’s dissertation project focuses on the role of HuR in the fibroblasts with a specific interest in cardiac fibrosis.

**Andrew J Kim, Ph.D** is currently completing his medical degree at Cincinnati Children’s Hospital Medical Center. Prior to this he worked in Katherine Yutzey’s laboratory within the Heart Institute, investigating how inflammation impacts the progression of heart valve disease by integrating the study of clinical specimens along with small and large animal models of valve disease.

**Jennifer Schwanekamp, Ph.D** is currently a Research Scientist on the Biomarker and Biomonitoring Team at UES, Inc. Prior to this she was a Postdoctoral Fellow in the Sadayappan lab under the NIH T32 training mechanism. As a postdoctoral trainee, she worked on understanding the molecular mechanism underlying hypertrophic cardiomyopathy resulting from mutations in MYBPC3.