Claudio Vinegoni, Ph.D. | Myocardial infarction accelerates atherosclerosis

Nature
Myocardial infarction accelerates atherosclerosis

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., 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., and Nahrendorf^#, M.

Nature 2012

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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.
@article{2012-NATURE, author= {Dutta, P. and Courties, G. and Wei, Y. and Leuschner, F. and Gorbatov, R. and Robbins, C. S. and Iwamoto, Y. and Thompson, B. and Carlson, A. L. and Heidt, T. and Majmudar, M. D. and Lasitschka, F. and Etzrodt, M. and Waterman, P. and Waring, M. T. and Chicoine, A. T. and van der Laan, A. M. and Niessen, H. W. M. and Piek, J. J. and Rubin, B. B. and Butany, J. and Stone, J. R. and Katus, H. A. and Murphy, S. A. and Morrow, D. A. and Sabatine, M. S. and Vinegoni, C. and Moskowitz, M. A. and Pittet, M. J. and Libby, P. and Lin, C. P. and Swirski, F. K. and Weissleder, R. and Nahrendorf<sup>#</sup>, M.}, title= {Myocardial infarction accelerates atherosclerosis}, journal= {Nature}, alternatejournal = {Nature}, year = {2012}, volume = {487}, number = {7407}, pages = {325-329}, issn = {0028-0836}, doi = {10.1038/nature11260}, pmcid = {PMC3401326}, pmid= {22763456} }
22763456

PMC3401326

10.1038/nature11260

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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For attribution in academic contexts, please cite this work as:

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, 487(7407), 325–329. https://doi.org/10.1038/nature11260