期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 321, 期 6, 页码 H1056-H1073出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00459.2021
关键词
cardiac; ischemia-reperfusion; myocardial infarction; rigor and reproducibility; rodent
资金
- National Institutes of Health [GM115458, HL137319, AA027625, HL136737, HL147570, HL076246, HL085440, HL149407, HL111600, HL122309, HL147844, GM127607, HL078825, HL132989, HL144788, HL145817, HL130972, HL127442, DK115213, HL136915, HL152297]
- Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development [BX000168, BX000505, BX003922]
- American Heart Association [IPA35260039, 18AIREA33960311, TPA2035490150]
- United States Department of Defense [PR181464]
- Natural Sciences Engineering Research Council [RGPIN-05520, RGPIN-04878]
- Canadian Institutes of Health Research [PJT-37522, PJT-153306, PJT-421341, PJo-413883]
- Canadian Foundation for Innovation [31708]
- Heart and Stroke Foundation of Canada [G-19-0026282, G-16-00014524]
- Heart and Stroke Foundation of New Brunswick
- National Health and Medical Research Council of Australia [APP1158013]
- New Brunswick Health Research and Innovation Foundations
This study evaluated different methods for inducing myocardial infarction in mouse models, identified opportunities for consolidating methods, and recognized that reperfused and nonreperfused myocardial infarctions yield different responses. The overall goal of compiling this consensus statement is to unify best practices regarding mouse myocardial infarction models to enhance interpretation and enable comparative examination across studies and laboratories. These guidelines aim to establish rigor and reproducibility, providing greater potential for clinical translation.
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.
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