The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Proliferation and Recruitment Contribute to Myocardial Macrophage Expansion in Chronic Heart Failure
Open accessAbstract
Rationale: Macrophages reside in the healthy myocardium, participate in ischemic heart disease, and modulate myocardial infarction (MI) healing. Their origin and roles in post-MI remodeling of nonischemic remote myocardium, however, remain unclear. Objective: This study investigated the number, origin, phenotype, and function of remote cardiac macrophages residing in the nonischemic myocardium in mice with chronic heart failure after coronary ligation. Methods and Results: Eight weeks post MI, fate mapping and flow cytometry revealed that a 2.9-fold increase in remote macrophages results from both increased local macrophage proliferation and monocyte recruitment. Heart failure produced by extensive MI, through activation of the sympathetic nervous system, expanded medullary and extramedullary hematopoiesis. Circulating Ly6C high monocytes rose from 64±5 to 108±9 per microliter of blood ( P <0.05). Cardiac monocyte recruitment declined in Ccr2 −/− mice, reducing macrophage numbers in the failing myocardium. Mechanical strain of primary murine and human macrophage cultures promoted cell cycle entry, suggesting that the increased wall tension in post-MI heart failure stimulates local macrophage proliferation. Strained cells activated the mitogen-activated protein kinase pathway, whereas specific inhibitors of this pathway reduced macrophage proliferation in strained cell cultures and in the failing myocardium ( P <0.05). Steady-state cardiac macrophages, monocyte-derived macrophages, and locally sourced macrophages isolated from failing myocardium expressed different genes in a pattern distinct from the M1/M2 macrophage polarization paradigm. In vivo silencing of endothelial cell adhesion molecules curbed post-MI monocyte recruitment to the remote myocardium and preserved ejection fraction (27.4±2.4 versus 19.1±2%; P <0.05). Conclusions: Myocardial failure is influenced by an altered myeloid cell repertoire.
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“Data on the abundance, origin, and function of macrophages are expanding rapidly.(64,65) Within the last decade, we”
Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure
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Self-citationIdentification of splenic reservoir monocytes and their deployment to inflammatory sites
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Self-citationRevisiting Cardiac Cellular Composition
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Cited by
Macrophages Facilitate Electrical Conduction in the Heart
Hulsmans, M., Clauss, S., Xiao, L., Aguirre, A. D., King, K. R., Hanley, A., Hucker, W. J., Wülfers, E. M., Seemann, G., Courties, G., et al. (2017) · Cell · doi:10.1016/j.cell.2017.03.050 · Cited by 1,011
Self-citationCardioimmunology: the immune system in cardiac homeostasis and disease
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Self-citationMacrophages in inflammation, repair and regeneration
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The human heart contains distinct macrophage subsets with divergent origins and functions
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Self-citationMechanically activated ion channel Piezo1 modulates macrophage polarization and stiffness sensing
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Metadata
- Authors
- Sager, H. B., Hulsmans, M., Lavine, K. J., Moreira, M. B., Heidt, T., Courties, G., Sun, Y., Iwamoto, Y., Tricot, B., Khan, O. F., Dahlman, J. E., Borodovsky, A., Fitzgerald, K., Anderson, D. G., Weissleder, R., Libby, P., Swirski, F. K., & Nahrendorf, M.
- Venue
- Circulation Research
- Published
- 2016-09-16
- Volume
- 119
- Issue
- 7
- Pages
- 853-864
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2479827938
- Cited by
- 415
- References
- 16
- FWCI
- 31.37
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Sager, H. B., Hulsmans, M., Lavine, K. J., Moreira, M. B., Heidt, T., Courties, G., Sun, Y., Iwamoto, Y., Tricot, B., Khan, O. F., Dahlman, J. E., Borodovsky, A., Fitzgerald, K., Anderson, D. G., Weissleder, R., Libby, P., Swirski, F. K., & Nahrendorf, M. (2016). Proliferation and Recruitment Contribute to Myocardial Macrophage Expansion in Chronic Heart Failure. Circulation Research. https://doi.org/10.1161/circresaha.116.309001
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
