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- Merry L. Lindsey
- Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, Omaha, Nebraska
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- Keith R. Brunt
- Department of Pharmacology, Faculty of Medicine, Dalhousie University, Saint John, New Brunswick, Canada
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- Jonathan A. Kirk
- Department of Cell and Molecular Physiology, Loyola University Chicago Stritch School of Medicine, Chicago, Illinois
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- Petra Kleinbongard
- Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, Essen, Germany
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- John W. Calvert
- Carlyle Fraser Heart Center of Emory University Hospital Midtown, Atlanta, Georgia
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- Lisandra E. de Castro Brás
- Department of Physiology, The Brody School of Medicine, East Carolina University, Greenville, North Carolina
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- Kristine Y. DeLeon-Pennell
- Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina
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- Dominic P. Del Re
- Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey
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- Nikolaos G. Frangogiannis
- Division of Cardiology, Department of Medicine, The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, New York
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- Stefan Frantz
- Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany
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- Richard J. Gumina
- Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio
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- Ganesh V. Halade
- Division of Cardiovascular Sciences, Department of Medicine, University of South Florida, Tampa, Florida
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- Steven P. Jones
- Department of Medicine, Diabetes and Obesity Center, University of Louisville, Louisville, Kentucky
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- Rebecca H. Ritchie
- Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University (Parkville Campus), Victoria, Australia
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- Francis G. Spinale
- Cardiovascular Translational Research Center, University of South Carolina School of Medicine and the Columbia Veteran Affairs Medical Center, Columbia, South Carolina
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- Edward B. Thorp
- Department of Pathology and Feinberg Cardiovascular and Renal Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
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- Crystal M. Ripplinger
- Department of Pharmacology, University of California Davis School of Medicine, Davis, California
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- Zamaneh Kassiri
- Department of Physiology, Cardiovascular Research Center, University of Alberta, Edmonton, Alberta, Canada
抄録
<jats:p> Despite significant improvements in reperfusion strategies, acute coronary syndromes all too often culminate in a myocardial infarction (MI). The consequent MI can, in turn, lead to remodeling of the left ventricle (LV), the development of LV dysfunction, and ultimately progression to heart failure (HF). Accordingly, an improved understanding of the underlying mechanisms of MI remodeling and progression to HF is necessary. One common approach to examine MI pathology is with murine models that recapitulate components of the clinical context of acute coronary syndrome and subsequent MI. We evaluated the different approaches used to produce MI in mouse models and identified opportunities to consolidate methods, recognizing that reperfused and nonreperfused MI yield different responses. The overall goal in compiling this consensus statement is to unify best practices regarding mouse MI models to improve interpretation and allow comparative examination across studies and laboratories. These guidelines will help to establish rigor and reproducibility and provide increased potential for clinical translation. </jats:p><jats:p> Listen to another corresponding podcast at https://ajpheart.podbean.com/e/guidelines-for-in-vivo-mouse-models-of-myocardial-infarction/ . </jats:p>
収録刊行物
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- American Journal of Physiology-Heart and Circulatory Physiology
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American Journal of Physiology-Heart and Circulatory Physiology 321 (6), H1056-H1073, 2021-12-01
American Physiological Society