Myocardial Infarction Accelerates Atherosclerosis

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Myocardial Infarction Accelerates Atherosclerosis

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Title: Myocardial Infarction Accelerates Atherosclerosis
Author: Leuschner, Florian; Robbins, Clinton; Iwamoto, Yoshiko; Thompson, Brian; Carlson, Alicia L.; Heidt, Timo; 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; Katus, Hugo A.; Murphy, Sabina A.; Pittet, Mikael J.; Lin, Charles P.; Dutta, Partha; Courties, Gabriel P; Wei, Ying; Gorbatov, Rostic; Majmudar, Maulik D; Stone, James Robert; Morrow, David Andrew; Sabatine, Marc Steven; Vinegoni, Claudio; Moskowitz, Michael Arthur; Libby, Peter; Swirski, Filip K.; Weissleder, Ralph; Nahrendorf, Matthias

Note: Order does not necessarily reflect citation order of authors.

Citation: Dutta, Partha, Gabriel Courties, Ying Wei, Florian Leuschner, Rostic Gorbatov, Clinton Robbins, Yoshiko Iwamoto, et al. 2012. Myocardial infarction accelerates atherosclerosis. Nature 487(7407): 325-329.
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Abstract: During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaque in the arterial wall and cause its 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 ischemic 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. When seeking the source of surplus monocytes in plaque, we found that myocardial infarction liberated hematopoietic stem and progenitor cells from bone marrow niches via sympathetic nervous system signaling. 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.
Published Version: doi:10.1038/nature11260
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401326/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10612854
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