ArticleAmerican journal of physiology. Heart and circulatory physiology2016
Defining the sham environment for post-myocardial infarction studies in mice.
Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 4 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 4 syntheses or guidelines pooled it, 33 citations in OpenAlex.
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- Guidelines for authors and reviewers on antibody use in physiology studies.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- IMproving Preclinical Assessment of Cardioprotective Therapies (IMPACT): a small animal acute myocardial infarction randomized-controlled multicenter study on the effect of ischemic preconditioning.Basic research in cardiology · 2025Article
- Prognostic value of the neutrophil percentage-to-albumin ratio for mortality in ICU patients with myocardial infarction: a retrospective cohort and machine learning analysis.Frontiers in cardiovascular medicine · 2025Article
- Enhanced neoangiogenesis and balance of the immune response mediated by the Wilms' tumor suppressor WT1 favor repair after myocardial infarction.Theranostics · 2025Article
- Article
- Guidelines on antibody use in physiology research.American journal of physiology. Renal physiology · 2024Article
- Histone modification landscape and the key significance of H3K27me3 in myocardial ischaemia/reperfusion injury.Science China. Life sciences · 2023Article
- Circulating lymphocyte trafficking to the bone marrow contributes to lymphopenia in myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2022Article
- Calcium and integrin binding protein 1 (CIB1) induces myocardial fibrosis in myocardial infarction via regulating the PI3K/Akt pathway.Experimental animals · 2022Article
- S100A9 is a functional effector of infarct wall thinning after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2022Article
- Sphingosine-1-phosphate interactions in the spleen and heart reflect extent of cardiac repair in mice and failing human hearts.American journal of physiology. Heart and circulatory physiology · 2021Article
- Article
- Exogenous IL-4 shuts off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to induce neutrophil phagocytosis following myocardial infarction.Journal of molecular and cellular cardiology · 2020Article
- Age- and sex-dependent differences in extracellular matrix metabolism associate with cardiac functional and structural changes.Journal of molecular and cellular cardiology · 2020Article
- Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesis.Basic research in cardiology · 2019Article
- Heart functional and structural compendium of cardiosplenic and cardiorenal networks in acute and chronic heart failure pathology.American journal of physiology. Heart and circulatory physiology · 2018Article
- Macrophage overexpression of matrix metalloproteinase-9 in aged mice improves diastolic physiology and cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2018Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
The purpose of this study was to evaluate the effect of sham surgery in a minimally invasive surgical model of permanent coronary artery occlusion used to generate myocardial infarction (MI) in mice. Adult male C57BL/6J mice (3-6 mo old) were divided into five groups: day (D) 0 (no surgical operation), D1 Sham, D1 MI, D7 Sham, and D7 MI. A refined MI surgery technique was used to approach the coronary artery without the ribs being cut. Both sham and MI mice had the left ventricle (LV) exposed through a small incision. To test the effects of surgery alone, the suture was passed around the coronary artery but not ligated. The MI mice were subjected to permanent coronary artery ligation. The mice were killed at D1 or D7 postsurgical procedure. Compared with D0 no surgery controls, the D1 and D7 sham groups exhibited no surgical mortality and similar necropsy and echocardiographic variables. Surgery alone did not induce an inflammatory cell response, as evidenced by the lack of leukocyte infiltration in the sham groups. Analysis of 165 inflammatory cytokines and extracellular matrix factors in sham revealed that a minor gene response was initiated but not translated to protein levels. Collagen deposition did not occur in the absence of MI. In contrast, the D1 and D7 MI groups showed the expected robust inflammatory and scar formation responses. When a minimally invasive procedure to generate MI in mice was used, the D0 (no surgical operation) control was an adequate replacement for the use of sham surgery groups.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.