ArticlePloS one2017
Apoptosis inhibitor of macrophage depletion decreased M1 macrophage accumulation and the incidence of cardiac rupture after myocardial infarction in mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Hepatic Mechanisms of Myocardial Infarction: A New Perspective in Metabolic Dysfunction-Associated Fatty Liver Disease.Journal of the American Heart Association · 2025Review
- Transforming heart transplantation care with multi-omics insights.Journal of translational medicine · 2025Review
- Endogenous CD5L controls the metabolic and inflammatory state of human macrophages.Frontiers in immunology · 2025Article
- Review
- Administration of an antibody against apoptosis inhibitor of macrophage prevents aortic aneurysm progression in mice.Scientific reports · 2024Article
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Single-cell analysis of uterosacral ligament revealed cellular heterogeneity in women with pelvic organ prolapse.Communications biology · 2024Article
- The effect of macrophages and their exosomes in ischemic heart disease.Frontiers in immunology · 2024Review
- Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression.Signal transduction and targeted therapy · 2023Article
- The comprehensive role of apoptosis inhibitor of macrophage (AIM) in pathological conditions.Clinical and experimental immunology · 2023Review
- Cardiac Myocyte-Specific Overexpression of FASTKD1 Prevents Ventricular Rupture After Myocardial Infarction.Journal of the American Heart Association · 2023Article
- Risk factors for cardiac rupture after acute ST-segment elevation myocardial infarction during the percutaneous coronary intervention era: a retrospective case-control study.Journal of thoracic disease · 2022Article
- Pathogenetic Link of Cardiac Rupture and Left Ventricular Thrombus Following Acute Myocardial Infarction: A Joint Preclinical and Clinical Study.Frontiers in cardiovascular medicine · 2022Article
- Article
- The effect of immune cell-derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre-clinical evidence.Journal of cellular and molecular medicine · 2021Review
- Apoptosis inhibitor of macrophage (AIM) contributes to IL-10-induced anti-inflammatory response through inhibition of inflammasome activation.Cell death & disease · 2021Article
- Oncostatin M promotes infarct repair and improves cardiac function after myocardial infarction.American journal of translational research · 2021Article
- Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of nonreperfused myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2020Article
- Human umbilical cord mesenchymal stem cells alleviate ongoing autoimmune dacryoadenitis in rabbits via polarizing macrophages into an anti-inflammatory phenotype.Experimental eye research · 2020Article
- Resveratrol improves cardiac function by promoting M2-like polarization of macrophages in mice with myocardial infarction.American journal of translational research · 2019Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac rupture is an important cause of death in the acute phase after myocardial infarction (MI). Macrophages play a pivotal role in cardiac remodeling after MI. Apoptosis inhibitor of macrophage (AIM) is secreted specifically by macrophages and contributes to macrophage accumulation in inflamed tissue by maintaining survival and recruiting macrophages. In this study, we evaluated the role of AIM in macrophage accumulation in the infarcted myocardium and cardiac rupture after MI. METHODS AND
resultsWild-type (WT) and AIM‒/‒ mice underwent permanent left coronary artery ligation and were followed-up for 7 days. Macrophage accumulation and phenotypes (M1 pro-inflammatory macrophage or M2 anti-inflammatory macrophage) were evaluated by immunohistological analysis and RT-PCR. Matrix metalloproteinase (MMP) activity levels were measured by gelatin zymography. The survival rate was significantly higher (81.1% vs. 48.2%, P<0.05), and the cardiac rupture rate was significantly lower in AIM‒/‒ mice than in WT mice (10.8% vs. 31.5%, P<0.05). The number of M1 macrophages and the expression levels of M1 markers (iNOS and IL-6) in the infarcted myocardium were significantly lower in AIM‒/‒ mice than in WT mice. In contrast, there was no difference in the number of M2 macrophages and the expression of M2 markers (Arg-1, CD206 and TGF-β1) between the two groups. The ratio of apoptotic macrophages in the total macrophages was significantly higher in AIM‒/‒ mice than in WT mice, although MCP-1 expression did not differ between the two groups. MMP-2 and 9 activity levels in the infarcted myocardium were significantly lower in AIM‒/‒ mice than in WT mice.
conclusionsThese findings suggest that AIM depletion decreases the levels of M1 macrophages, which are a potent source of MMP-2 and 9, in the infarcted myocardium in the acute phase after MI by promoting macrophage apoptosis, and leads to a decrease in the incidence of cardiac rupture and improvements in survival rates.
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