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Cited by 1,079

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Myocardial infarction accelerates atherosclerosis

Open access
Dutta, Partha, Courties, Gabriel, Wei, Ying, Leuschner, Florian, Gorbatov, Rostic, Robbins, Clinton S., Iwamoto, Yoshiko, Thompson, Brian, Carlson, Alicia L., Heidt, Timo, Majmudar, Maulik D., Lasitschka, Felix, Etzrodt, Martin, Waterman, Peter, Waring, Michael T., Chicoine, Adam T., van der Laan, Anja M., Niessen, Hans W. M., Piek, Jan J., Rubin, Barry B., Butany, Jagdish, Stone, James R., Katus, Hugo A., Murphy, Sabina A., Morrow, David A., Sabatine, Marc S., Vinegoni, Claudio, Moskowitz, Michael A., Pittet, Mikael J., Libby, Peter, Lin, Charles P., Swirski, Filip K., Weissleder, Ralph, Nahrendorf, Matthias·2012·Nature
DOI 10.1038/nature11260
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Abstract

During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaques in the arterial wall and cause their rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. Here we show that the systemic response to ischaemic injury aggravates chronic atherosclerosis. After myocardial infarction or stroke, Apoe−/− mice developed larger atherosclerotic lesions with a more advanced morphology. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment. Seeking the source of surplus monocytes in plaques, we found that myocardial infarction liberated haematopoietic stem and progenitor cells from bone marrow niches via sympathetic nervous system signalling. The progenitors then seeded the spleen, yielding a sustained boost in monocyte production. These observations provide new mechanistic insight into atherogenesis and provide a novel therapeutic opportunity to mitigate disease progression.

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Metadata

Authors
Dutta, P., Courties, G., Wei, Y., Leuschner, F., Gorbatov, R., Robbins, C. S., Iwamoto, Y., Thompson, B., Carlson, A. L., Heidt, T., Majmudar, M. D., Lasitschka, F., Etzrodt, M., Waterman, P., Waring, M. T., Chicoine, A. T., van der Laan, A. M., Niessen, H. W. M., Piek, J. J., Rubin, B. B., Butany, J., Stone, J. R., Katus, H. A., Murphy, S. A., Morrow, D. A., Sabatine, M. S., Vinegoni, C., Moskowitz, M. A., Pittet, M. J., Libby, P., Lin, C. P., Swirski, F. K., Weissleder, R., & Nahrendorf, M.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2012-06-27
Volume
487
Issue
7407
Pages
325-329
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/nature11260
OpenAlex
W2099172760
Cited by
1,079
References
8
FWCI
31.43
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Myocardial infarction accelerates atherosclerosis. https://app.cochat.ai/papers/10.1038/nature11260
The paper
Dutta, P., Courties, G., Wei, Y., Leuschner, F., Gorbatov, R., Robbins, C. S., Iwamoto, Y., Thompson, B., Carlson, A. L., Heidt, T., Majmudar, M. D., Lasitschka, F., Etzrodt, M., Waterman, P., Waring, M. T., Chicoine, A. T., van der Laan, A. M., Niessen, H. W. M., Piek, J. J., . . . Nahrendorf, M. (2012). Myocardial infarction accelerates atherosclerosis. Nature. https://doi.org/10.1038/nature11260

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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.