Myocardial infarction accelerates atherosclerosis
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 sy...
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| Main Authors: | , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
27 June 2012
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| In: |
Nature
Year: 2012, Volume: 487, Issue: 7407, Pages: 325-329 |
| ISSN: | 1476-4687 |
| DOI: | 10.1038/nature11260 |
| Online Access: | Verlag, Volltext: https://doi.org/10.1038/nature11260 Verlag, Volltext: https://www.nature.com/articles/nature11260 
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| Author Notes: | Partha Dutta, Gabriel Courties, Ying Wei, Florian Leuschner, Rostic Gorbatov, Clinton S. Robbins, Yoshiko Iwamoto, Brian Thompson, Alicia L. Carlson, Timo Heidt, Maulik D. Majmudar, Felix Lasitschka, Martin Etzrodt, Peter Waterman, Michael T. Waring, Adam T. Chicoine, Anja M. van der Laan, Hans W.M. Niessen, Jan J. Piek, Barry B. Rubin, Jagdish Butany, James R. Stone, Hugo A. Katus, Sabina A. Murphy, David A. Morrow, Marc S. Sabatine, Claudio Vinegoni, Michael A. Moskowitz, Mikael J. Pittet, Peter Libby, Charles P. Lin, Filip K. Swirski, Ralph Weissleder & Matthias Nahrendorf |
MARC
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| 520 | |a 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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