Myocardial infarction accelerates atherosclerosis

By Partha Dutta, G. Courties, Ying Wei, F. Leuschner, Rostic Gorbatov, Clinton S. Robbins, Y. Iwamoto, B. Thompson, Alicia L. Carlson, T. Heidt and 24 more. Nature, 2012

1,053 citations recorded by the source corpus.

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.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/baf3ef20ccce1a9675ad89debf99098da0213a05

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Citations in the corpus

Immune Effector Mechanisms Implicated in Atherosclerosis: From Mice to Humans (2013, background): “Cells from this splenic population home to sites of acute injury, such as infarcts of the heart or brain, as well as to sites of chronic inflammation, such as atheroma in mice (Dutta et al., 2012).”
The spleen in local and systemic regulation of immunity (2013, background): “These include cytokines and soluble molecules (thrombospondin, TGFb, IL-10), membrane-boundmolecules (TRAIL and programmed death ligand 1 [PD-L1]), enzymes (IDO, ARG, NOS, and 12/15 lipoxigenase [12/15 LO]) and reactive oxygen species (ROS).”
Oxidized Low-Density Lipoprotein Induces Long-Term Proinflammatory Cytokine Production and Foam Cell Formation via Epigenetic Reprogramming of Monocytes (2014, background): “infarction can accelerate atherogenesis by changing the number and characteristics of circulating monocytes.(9,10) Although”
Imaging macrophages with nanoparticles. (2014, methodology): “Imaging TAMs could thus be used to (1) provide prognostic information, (2) visualize differences in TAM concentrations within a single tumour or across metastases, (3) guide biopsies, (4) define tumour margins101,119 and (5) quantitate responses to treatment by mapping apoptosis-initiated macrophage”
Chronic variable stress activates hematopoietic stem cells (2014, neutral): “To inhibit β 3 adrenergic signaling, a specific antagonist for the adrenergic receptor β 3 (SR 59230A, Sigma–Aldrich) was injected at 5 mg/kg i.p. twice per day 43 .”