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Cited by 209

The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.

The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes

Open access
Anzai, Atsushi, Choi, Jennifer L., He, Shun, Fenn, Ashley M., Nairz, Manfred, Rattik, Sara, McAlpine, Cameron S., Mindur, John E., Chan, Christopher T., Iwamoto, Yoshiko, Tricot, Benoit, Wojtkiewicz, Gregory R., Weissleder, Ralph, Libby, Peter, Nahrendorf, Matthias, Stone, James R., Becher, Burkhard, Swirski, Filip K.·2017·Journal of Experimental Medicine

Abstract

Myocardial infarction (MI) elicits massive inflammatory leukocyte recruitment to the heart. Here, we hypothesized that excessive leukocyte invasion leads to heart failure and death during acute myocardial ischemia. We found that shortly and transiently after onset of ischemia, human and mouse cardiac fibroblasts produce granulocyte/macrophage colony-stimulating factor (GM-CSF) that acts locally and distally to generate and recruit inflammatory and proteolytic cells. In the heart, fibroblast-derived GM-CSF alerts its neighboring myeloid cells to attract neutrophils and monocytes. The growth factor also reaches the bone marrow, where it stimulates a distinct myeloid-biased progenitor subset. Consequently, hearts of mice deficient in either GM-CSF or its receptor recruit fewer leukocytes and function relatively well, whereas mice producing GM-CSF can succumb from left ventricular rupture, a complication mitigated by anti–GM-CSF therapy. These results identify GM-CSF as both a key contributor to the pathogenesis of MI and a potential therapeutic target, bolstering the idea that GM-CSF is a major orchestrator of the leukocyte supply chain during inflammation.

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Metadata

Authors
Anzai, A., Choi, J. L., He, S., Fenn, A. M., Nairz, M., Rattik, S., McAlpine, C. S., Mindur, J. E., Chan, C. T., Iwamoto, Y., Tricot, B., Wojtkiewicz, G. R., Weissleder, R., Libby, P., Nahrendorf, M., Stone, J. R., Becher, B., & Swirski, F. K.
Venue
Journal of Experimental Medicine
Published
2017-10-04
Volume
214
Issue
11
Pages
3293-3310
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2762754852
Cited by
209
References
10
FWCI
15.22
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes. https://app.cochat.ai/papers/10.1084/jem.20170689
The paper
Anzai, A., Choi, J. L., He, S., Fenn, A. M., Nairz, M., Rattik, S., McAlpine, C. S., Mindur, J. E., Chan, C. T., Iwamoto, Y., Tricot, B., Wojtkiewicz, G. R., Weissleder, R., Libby, P., Nahrendorf, M., Stone, J. R., Becher, B., & Swirski, F. K. (2017). The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20170689

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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.