Guidelines for in vivo mouse models of myocardial infarction.

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. Accordingly, improved understanding of the underlying mechanisms of MI remodeling and progression to heart failure 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 non-reperfused 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.

[1]  A. Engler,et al.  Regenerative Crosstalk between Cardiac Cells and Macrophages. , 2021, American journal of physiology. Heart and circulatory physiology.

[2]  C. Emter,et al.  Large Animal Models of Heart Failure , 2020, JACC. Basic to translational science.

[3]  T. Nakajima,et al.  Inhibition of xanthine oxidase in the acute phase of myocardial infarction prevents skeletal muscle abnormalities and exercise intolerance. , 2020, Cardiovascular research.

[4]  A. Feldman,et al.  Cardiomyocyte contractile impairment in heart failure results from reduced BAG3-mediated sarcomeric protein turnover , 2020, Nature Communications.

[5]  S. Houser,et al.  Cortical bone derived stem-cell therapy reduces apoptosis after myocardial infarction. , 2019, American journal of physiology. Heart and circulatory physiology.

[6]  Michael E. Hall,et al.  Identifying the molecular and cellular signature of cardiac dilation following myocardial infarction. , 2019, Biochimica et biophysica acta. Molecular basis of disease.

[7]  G. Wright,et al.  Human Embryonic Stem Cell-Derived Cardiomyocytes Regenerate the Infarcted Pig Heart but Induce Ventricular Tachyarrhythmias , 2019, Stem cell reports.

[8]  J. Walsh,et al.  Cardioprotective Actions of the Annexin-A1 N-Terminal Peptide, Ac2-26, Against Myocardial Infarction , 2019, Front. Pharmacol..

[9]  Amanda B. Pullen,et al.  Pretreatment of carprofen impaired initiation of inflammatory‐ and overlapping resolution response and promoted cardiorenal syndrome in heart failure , 2019, Life sciences.

[10]  E. Gao,et al.  Resistin promotes cardiac homing of mesenchymal stem cells and functional recovery after myocardial ischemia-reperfusion via the ERK1/2-MMP-9 pathway. , 2019, American journal of physiology. Heart and circulatory physiology.

[11]  F. Ginhoux,et al.  Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction , 2018, Nature Immunology.

[12]  Josephine C. Adams,et al.  Revised guidelines to enhance the rigor and reproducibility of research published in American Physiological Society journals. , 2018, American journal of physiology. Regulatory, integrative and comparative physiology.

[13]  Guogang Zhang,et al.  A minimally invasive approach to induce myocardial infarction in mice without thoracotomy , 2018, Journal of cellular and molecular medicine.

[14]  M. Lindsey,et al.  Mapping macrophage polarization over the myocardial infarction time continuum , 2018, Basic Research in Cardiology.

[15]  M. Volpe,et al.  Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction. , 2018, Journal of the American College of Cardiology.

[16]  J. Ferreira,et al.  Inclusion and exclusion criteria in research studies: definitions and why they matter , 2018, Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia.

[17]  E. Chepurko,et al.  Impact of cardiac‐specific expression of CD39 on myocardial infarct size in mice , 2017, Life sciences.

[18]  P. Sexton,et al.  Small-molecule-biased formyl peptide receptor agonist compound 17b protects against myocardial ischaemia-reperfusion injury in mice , 2017, Nature Communications.

[19]  R. Graham,et al.  IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction , 2016, Proceedings of the National Academy of Sciences.

[20]  Courtney A Cates,et al.  Temporal neutrophil polarization following myocardial infarction. , 2016, Cardiovascular research.

[21]  Pallav Sengupta,et al.  Men and mice: Relating their ages. , 2016, Life sciences.

[22]  P. Doevendans,et al.  Translational failure of anti-inflammatory compounds for myocardial infarction: a meta-analysis of large animal models. , 2016, Cardiovascular research.

[23]  M. Lindsey,et al.  Early matrix metalloproteinase-12 inhibition worsens post-myocardial infarction cardiac dysfunction by delaying inflammation resolution. , 2015, International journal of cardiology.

[24]  J. Ioannidis,et al.  Reproducibility in Science: Improving the Standard for Basic and Preclinical Research , 2015, Circulation research.

[25]  Eric T. Wang,et al.  Alternative splicing regulates vesicular trafficking genes in cardiomyocytes during postnatal heart development , 2014, Nature Communications.

[26]  David Handelsman,et al.  Role of androgens in sex differences in cardiac damage during myocardial infarction. , 2014, Endocrinology.

[27]  E. Olson,et al.  Surgical models for cardiac regeneration in neonatal mice , 2014, Nature Protocols.

[28]  Gregory M. Fomovsky,et al.  Regional mechanics determine collagen fiber structure in healing myocardial infarcts. , 2012, Journal of molecular and cellular cardiology.

[29]  C. Begley,et al.  Drug development: Raise standards for preclinical cancer research , 2012, Nature.

[30]  J. Zweier,et al.  Transgenic over expression of ectonucleotide triphosphate diphosphohydrolase-1 protects against murine myocardial ischemic injury. , 2011, Journal of molecular and cellular cardiology.

[31]  F. Prinz,et al.  Believe it or not: how much can we rely on published data on potential drug targets? , 2011, Nature Reviews Drug Discovery.

[32]  G. Heusch,et al.  The in-situ pig heart with regional ischemia/reperfusion - ready for translation. , 2011, Journal of molecular and cellular cardiology.

[33]  D G Altman,et al.  Improving bioscience research reporting: ARRIVE-ing at a solution , 2010, Laboratory animals.

[34]  Bruce M. Psaty,et al.  Minimizing bias in randomized trials: the importance of blinding. , 2010, JAMA.

[35]  J. Brophy,et al.  Association between timeliness of reperfusion therapy and clinical outcomes in ST-elevation myocardial infarction. , 2010, JAMA.

[36]  F. Dekker,et al.  Sample size calculations: basic principles and common pitfalls. , 2010, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.

[37]  R. Gu,et al.  Thrombin and Its Receptor Enhance ST-Segment Elevation in Acute Myocardial Infarction by Activating the KATP Channel , 2010, Molecular medicine.

[38]  L. Maia,et al.  The use of lidocaine as an anti-inflammatory substance: a systematic review. , 2009, Journal of dentistry.

[39]  R. Porcher,et al.  Statistics in Brief: The Importance of Sample Size in the Planning and Interpretation of Medical Research , 2008, Clinical orthopaedics and related research.

[40]  P. Libby,et al.  The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions , 2007, The Journal of experimental medicine.

[41]  M. Entman,et al.  The role of platelet-derived growth factor signaling in healing myocardial infarcts. , 2006, Journal of the American College of Cardiology.

[42]  M. Harmsen,et al.  Increased inflammatory response and neovascularization in reperfused vs. non-reperfused murine myocardial infarction. , 2006, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

[43]  Joon Beom Seo,et al.  MR imaging of reperfused myocardial infarction: comparison of necrosis-specific and intravascular contrast agents in a cat model. , 2003, Radiology.

[44]  R. Kloner,et al.  No-reflow phenomenon. , 2002, Circulation.

[45]  D. Volker,et al.  Oral buprenorphine is anti-inflammatory and modulates the pathogenesis of streptococcal cell wall polymer-induced arthritis in the Lew/SSN rat , 2000, Laboratory animals.

[46]  T. McKean,et al.  Comparison of the responses to hypoxia, ischaemia and ischaemic preconditioning in wild marmot and laboratory rabbit hearts. , 1996, The Journal of experimental biology.

[47]  S. Kusachi,et al.  Reperfusion hastens appearance and extent of distribution of type I collagen in infarct zone: immunohistochemical study in rat experimental infarction. , 1995, Cardiovascular research.

[48]  M. Pfeffer,et al.  Ventricular Remodeling After Myocardial Infarction: Experimental Observations and Clinical Implications , 1990, Circulation.

[49]  J. Roberts,et al.  The cat as a model for myocardial infarction. , 1979, Cardiovascular research.

[50]  J. Roberts,et al.  Comparison of the arrhythmogenic effect of myocardial infarction in the cat and dog. , 1979, Cardiovascular research.

[51]  O. Cingolani,et al.  Thrombospondins in the transition from myocardial infarction to heart failure. , 2016, Journal of molecular and cellular cardiology.

[52]  R. Gourdie,et al.  Cryoinjury models of the adult and neonatal mouse heart for studies of scarring and regeneration. , 2013, Methods in molecular biology.

[53]  E. Thorp,et al.  Quantitation of acute necrosis after experimental myocardial infarction. , 2013, Methods in molecular biology.

[54]  M. Lindsey,et al.  Cardiac wound healing post-myocardial infarction: a novel method to target extracellular matrix remodeling in the left ventricle. , 2013, Methods in molecular biology.

[55]  M. Ruiz-Meana,et al.  Animal ethics in Cardiovascular Research. , 2012, Cardiovascular research.

[56]  M. Harmsen,et al.  Cryoinjury: a model of myocardial regeneration. , 2008, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

[57]  K. Murray,et al.  Phenotyping of genetically engineered mice: humane, ethical, environmental, and husbandry issues. , 2006, ILAR journal.