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Myocardial infarction accelerates atherosclerosis

Author

Listed:
  • Partha Dutta

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Gabriel Courties

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Ying Wei

    (Stroke and Neurovascular Regulation Laboratory, Massachusetts General Hospital/Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA)

  • Florian Leuschner

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
    Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, D-69120 Heidelberg, Germany)

  • Rostic Gorbatov

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Clinton S. Robbins

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Yoshiko Iwamoto

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Brian Thompson

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Alicia L. Carlson

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Timo Heidt

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Maulik D. Majmudar

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
    Brigham and Women’s Hospital)

  • Felix Lasitschka

    (Institute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 220/221, 69120 Heidelberg, Germany)

  • Martin Etzrodt

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Peter Waterman

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Michael T. Waring

    (The Ragon Institute of MGH, MIT and Harvard at Massachusetts General Hospital
    Howard Hughes Medical Institute)

  • Adam T. Chicoine

    (The Ragon Institute of MGH, MIT and Harvard at Massachusetts General Hospital
    Howard Hughes Medical Institute)

  • Anja M. van der Laan

    (Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, the Netherlands)

  • Hans W. M. Niessen

    (ICaR-VU, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, the Netherlands)

  • Jan J. Piek

    (Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, the Netherlands)

  • Barry B. Rubin

    (Peter Munk Cardiac Centre, Toronto General Hospital, University of Toronto, Toronto, Ontario M5G-2C4, Canada)

  • Jagdish Butany

    (Peter Munk Cardiac Centre, University of Toronto, Toronto, Ontario M5G-2C4, Canada)

  • James R. Stone

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
    Massachusetts General Hospital and Harvard Medical School)

  • Hugo A. Katus

    (Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, D-69120 Heidelberg, Germany)

  • Sabina A. Murphy

    (TIMI Study Group, Brigham and Women’s Hospital)

  • David A. Morrow

    (TIMI Study Group, Brigham and Women’s Hospital)

  • Marc S. Sabatine

    (TIMI Study Group, Brigham and Women’s Hospital)

  • Claudio Vinegoni

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Michael A. Moskowitz

    (Stroke and Neurovascular Regulation Laboratory, Massachusetts General Hospital/Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA)

  • Mikael J. Pittet

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Peter Libby

    (Brigham and Women’s Hospital)

  • Charles P. Lin

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Filip K. Swirski

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

  • Ralph Weissleder

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA
    Harvard Medical School)

  • Matthias Nahrendorf

    (Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, Massachusetts 02114, USA)

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.

Suggested Citation

  • 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 L, 2012. "Myocardial infarction accelerates atherosclerosis," Nature, Nature, vol. 487(7407), pages 325-329, July.
    • Handle: RePEc:nat:nature:v:487:y:2012:i:7407:d:10.1038_nature11260
    DOI: 10.1038/nature11260
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    Citations

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    Cited by:

    1. Yu-Jung Tseng & Yuki Kageyama & Rebecca L. Murdaugh & Ayumi Kitano & Jong Hwan Kim & Kevin A. Hoegenauer & Jonathan Tiessen & Mackenzie H. Smith & Hidetaka Uryu & Koichi Takahashi & James F. Martin & , 2024. "Increased iron uptake by splenic hematopoietic stem cells promotes TET2-dependent erythroid regeneration," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    2. Chu-Chih Chen & , Chuan-Pin Lee & Yuan-Horng Yan & Tsun-Jen Cheng & Pranab K. Sen, 2021. "A partial likelihood-based two-dimensional multistate markov model with application to myocardial infarction and stroke recurrence," Sankhya B: The Indian Journal of Statistics, Springer;Indian Statistical Institute, vol. 83(2), pages 282-303, November.
    3. Thi Tran & Jean-Remi Lavillegrand & Cedric Lereverend & Bruno Esposito & Lucille Cartier & Melanie Montabord & Jaouen Tran-Rajau & Marc Diedisheim & Nadège Gruel & Khadija Ouguerram & Lea Paolini & Ol, 2022. "Mild dyslipidemia accelerates tumorigenesis through expansion of Ly6Chi monocytes and differentiation to pro-angiogenic myeloid cells," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    4. Hung-Jui Hsu & Chia-Yi Lee & Shih-Chun Chao & Chan-Wei Nien & Shih-Hao Tzeng & Jing-Yang Huang & Tai-Chuan Ko & Shun-Fa Yang & Hung-Yu Lin, 2019. "The Correlation of Central Serous Chorioretinopathy and Subsequent Cardiovascular Diseases of Different Types: A Population-Based Cohort Study," IJERPH, MDPI, vol. 16(24), pages 1-10, December.

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