Myocardial infarction accelerates atherosclerosis

被引：867

作者：

Dutta, Partha ^{[1
,2
]}

Courties, Gabriel ^{[1
,2
]}

Wei, Ying ^{[3
,4
]}

Leuschner, Florian ^{[1
,2
,5
]}

Gorbatov, Rostic ^{[1
,2
]}

Robbins, Clinton S. ^{[1
,2
]}

Iwamoto, Yoshiko ^{[1
,2
]}

Thompson, Brian ^{[1
,2
]}

Carlson, Alicia L. ^{[1
,2
]}

Heidt, Timo ^{[1
,2
]}

Majmudar, Maulik D. ^{[1
,2
,6
]}

Lasitschka, Felix ^{[7
]}

Etzrodt, Martin ^{[1
,2
]}

Waterman, Peter ^{[1
,2
]}

Waring, Michael T. ^{[8
,9
]}

Chicoine, Adam T. ^{[8
,9
]}

van der Laan, Anja M. ^{[10
]}

Niessen, Hans W. M. ^{[11
]}

Piek, Jan J. ^{[10
]}

Rubin, Barry B. ^{[12
]}

Butany, Jagdish ^{[13
]}

Stone, James R. ^{[1
,2
,14
]}

Katus, Hugo A. ^{[5
]}

Murphy, Sabina A. ^{[15
]}

Morrow, David A. ^{[15
]}

Sabatine, Marc S. ^{[15
]}

Vinegoni, Claudio ^{[1
,2
]}

Moskowitz, Michael A. ^{[3
,4
]}

Pittet, Mikael J. ^{[1
,2
]}

Libby, Peter ^{[6
]}

Lin, Charles P. ^{[1
,2
]}

Swirski, Filip K. ^{[1
,2
]}

Weissleder, Ralph ^{[1
,2
,16
]}

Nahrendorf, Matthias ^{[1
,2
]}

机构：

[1] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA

[2] Harvard Univ, Sch Med, Boston, MA 02114 USA

[3] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,Stroke & Neurovasc Regulat Lab, Charlestown, MA 02129 USA

[4] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol,Stroke & Neurovasc Regulat Lab, Charlestown, MA 02129 USA

[5] Med Univ Hosp Heidelberg, Dept Cardiol, D-69120 Heidelberg, Germany

[6] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA

[7] Univ Heidelberg Hosp, Inst Pathol, D-69120 Heidelberg, Germany

[8] MIT & Harvard Massachusetts Gen Hosp, Ragon Inst MGH, Charlestown, MA 02129 USA

[9] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA

[10] Univ Amsterdam, Acad Med Ctr, Dept Cardiol, NL-1105 AZ Amsterdam, Netherlands

[11] Vrije Univ Amsterdam Med Ctr, ICaR VU, Dept Pathol & Cardiac Surg, NL-1081 HV Amsterdam, Netherlands

[12] Univ Toronto, Toronto Gen Hosp, Peter Munk Cardiac Ctr, Div Vasc Surg, Toronto, ON M5G 2C4, Canada

[13] Univ Toronto, Peter Munk Cardiac Ctr, Dept Pathol, Toronto, ON M5G 2C4, Canada

[14] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA

[15] Brigham & Womens Hosp, Div Cardiovasc, Dept Med, TIMI Study Grp, Boston, MA 02145 USA

[16] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA

来源：

NATURE | 2012年 / 487卷 / 7407期

关键词：

HEMATOPOIETIC STEM-CELLS; ACUTE CORONARY SYNDROMES; MONOCYTE SUBSETS; PROGENITOR CELLS; ARTERY-DISEASE; BONE-MARROW; INFLAMMATION; PLAQUES; NICHE; IDENTIFICATION;

D O I：

10.1038/nature11260

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：325 / 329

页数：5

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