The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Monocytes/macrophages prevent healing defects and left ventricular thrombus formation after myocardial infarction
Abstract
Myocardial infarction (MI) leads to rapid necrosis of cardiac myocytes. To achieve tissue integrity and function, inflammatory cells are activated, including monocytes/macrophages. However, the effect of monocyte/macrophage recruitment after MI remains poorly defined. After experimental MI, monocytes and macrophages were depleted through serial injections of clodronate‐containing liposomes. Monocyte/macrophage infiltration was reduced in the myocardium after MI by active treatment. Mortality was increased due to thromboembolic events in monocyte‐ and macrophage‐depleted animals (92 vs. 33%; P <0.01). Left ventricular thrombi were detectable as early as 24 h after MI; this was reproduced in a genetic model of monocyte/macrophage ablation. A general prothrombotic state, increased infarct expansion, and deficient neovascularization were not observed. Severely compromised extracellular matrix remodeling (collagen I, placebo liposome vs. clodronate liposome, 2.4±0.2 vs. 0.8±0.2 arbitrary units; P <0.001) and locally lost integrity of the endocardium after MI are potential mechanisms. Patients with a left ventricular thrombus had a relative decrease of CD14 + CD16 + monocyte/macrophage subsets in the peripheral blood after MI (no thrombus vs. thrombus, 14.2±0.9 vs. 7.80±0.4%; P <0.05). In summary, monocytes/macrophages are of central importance for healing after MI. Impaired monocyte/macrophage function appears to be an unrecognized new pathophysiological mechanism for left ventricular thrombus development after MI.—Frantz, S., Hofmann, U., Fraccarollo, D., Schäfer, A., Kranepuhl, S., Hagedorn, I., Nieswandt, B., Nahrendorf, M., Wagner, H., Bayer, B., Pachel, C., Schön, M.P., Kneitz, S., Bobinger, T., Weidemann, F., Ertl, G., Bauersachs, J. Monocytes/macrophages prevent healing defects and left ventricular thrombus formation after myocardial infarction. FASEB J. 27, 871–881 (2013). www.fasebj.org
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Nahrendorf, M., Swirski, F. K., Aikawa, E., Stangenberg, L., Wurdinger, T., Figueiredo, J.-L., Libby, P., Weissleder, R., & Pittet, M. J. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070885 · Cited by 2,300
Self-citationDifferential Roles of Macrophages in Diverse Phases of Skin Repair
Lucas, T., Waisman, A., Ranjan, R., Roes, J., Krieg, T., Müller, W., Roers, A., & Eming, S. A. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0903356 · Cited by 1,205 · cited 2×
“To confirm that these effects are not a treatment artifact, we used LysMCre/iDTR mice (n 7) in which diphtheria toxin can efficiently and specifically deplete tissue-resident and inflammatory monocytes/macrophages (8).”
Methodvan Amerongen, M. J., Harmsen, M. C., van Rooijen, N., Petersen, A. H., & van Luyn, M. J. A. (2007) · The American Journal of Pathology · doi:10.2353/ajpath.2007.060547 · Cited by 544
Cited by
Macrophages in inflammation, repair and regeneration
Oishi, Y., & Manabe, I. (2018) · International Immunology · doi:10.1093/intimm/dxy054 · Cited by 734
Ma, Y., Mouton, A. J., & Lindsey, M. L. (2018) · Translational Research · doi:10.1016/j.trsl.2017.10.001 · Cited by 405
Nonclassical Patrolling Monocyte Function in the Vasculature
Thomas, G., Tacke, R., Hedrick, C. C., & Hanna, R. N. (2015) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.114.304650 · Cited by 367
Inflammation in acute myocardial infarction: the good, the bad and the ugly
Matter, M. A., Paneni, F., Libby, P., Frantz, S., Stähli, B. E., Templin, C., Mengozzi, A., Wang, Y.-J., Kündig, T. M., Räber, L., et al. (2024) · European Heart Journal · doi:10.1093/eurheartj/ehad486 · Cited by 357
Self-citationCardiac macrophages and their role in ischaemic heart disease
Frantz, S., & Nahrendorf, M. (2014) · Cardiovascular Research · doi:10.1093/cvr/cvu025 · Cited by 310
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Metadata
- Authors
- Frantz, S., Hofmann, U., Fraccarollo, D., Schäfer, A., Kranepuhl, S., Hagedorn, I., Nieswandt, B., Nahrendorf, M., Wagner, H., Bayer, B., Pachel, C., Schön, M. P., Kneitz, S., Bobinger, T., Weidemann, F., Ertl, G., & Bauersachs, J.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2012-11-16
- Volume
- 27
- Issue
- 3
- Pages
- 871-881
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2004945550
- Cited by
- 195
- References
- 3
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- closed
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- Frantz, S., Hofmann, U., Fraccarollo, D., Schäfer, A., Kranepuhl, S., Hagedorn, I., Nieswandt, B., Nahrendorf, M., Wagner, H., Bayer, B., Pachel, C., Schön, M. P., Kneitz, S., Bobinger, T., Weidemann, F., Ertl, G., & Bauersachs, J. (2013). Monocytes/macrophages prevent healing defects and left ventricular thrombus formation after myocardial infarction. The FASEB Journal. https://doi.org/10.1096/fj.12-214049
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
