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Cited by 521

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis

Open access
Leuschner, Florian, Rauch, Philipp J., Ueno, Takuya, Gorbatov, Rostic, Marinelli, Brett, Lee, Won Woo, Dutta, Partha, Wei, Ying, Robbins, Clinton, Iwamoto, Yoshiko, Sena, Brena, Chudnovskiy, Aleksey, Panizzi, Peter, Keliher, Edmund, Higgins, John M., Libby, Peter, Moskowitz, Michael A., Pittet, Mikael J., Swirski, Filip K., Weissleder, Ralph, Nahrendorf, Matthias·2012·Journal of Experimental Medicine

Abstract

Monocytes (Mo) and macrophages (MΦ) are emerging therapeutic targets in malignant, cardiovascular, and autoimmune disorders. Targeting of Mo/MΦ and their effector functions without compromising innate immunity’s critical defense mechanisms first requires addressing gaps in knowledge about the life cycle of these cells. Here we studied the source, tissue kinetics, and clearance of Mo/MΦ in murine myocardial infarction, a model of acute inflammation after ischemic injury. We found that a) Mo tissue residence time was surprisingly short (20 h); b) Mo recruitment rates were consistently high even days after initiation of inflammation; c) the sustained need of newly made Mo was fostered by extramedullary monocytopoiesis in the spleen; d) splenic monocytopoiesis was regulated by IL-1β; and e) the balance of cell recruitment and local death shifted during resolution of inflammation. Depending on the experimental approach, we measured a 24 h Mo/MΦ exit rate from infarct tissue between 5 and 13% of the tissue cell population. Exited cells were most numerous in the blood, liver, and spleen. Abrogation of extramedullary monocytopoiesis proved deleterious for infarct healing and accelerated the evolution of heart failure. We also detected rapid Mo kinetics in mice with stroke. These findings expand our knowledge of Mo/MΦ flux in acute inflammation and provide the groundwork for novel anti-inflammatory strategies for treating heart failure.

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Metadata

Authors
Leuschner, F., Rauch, P. J., Ueno, T., Gorbatov, R., Marinelli, B., Lee, W. W., Dutta, P., Wei, Y., Robbins, C., Iwamoto, Y., Sena, B., Chudnovskiy, A., Panizzi, P., Keliher, E., Higgins, J. M., Libby, P., Moskowitz, M. A., Pittet, M. J., Swirski, F. K., Weissleder, R., & Nahrendorf, M.
Venue
Journal of Experimental Medicine
Published
2012-01-02
Volume
209
Issue
1
Pages
123-137
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2119610102
Cited by
521
References
9
FWCI
29.35
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis. https://app.cochat.ai/papers/10.1084/jem.20111009
The paper
Leuschner, F., Rauch, P. J., Ueno, T., Gorbatov, R., Marinelli, B., Lee, W. W., Dutta, P., Wei, Y., Robbins, C., Iwamoto, Y., Sena, B., Chudnovskiy, A., Panizzi, P., Keliher, E., Higgins, J. M., Libby, P., Moskowitz, M. A., Pittet, M. J., Swirski, F. K., . . . Nahrendorf, M. (2012). Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20111009

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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.