The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
Macrophages in vascular inflammation – From atherosclerosis to vasculitis
Open accessAbstract
The spectrum of vascular inflammatory disease ranges from atherosclerosis and hypertension, widespread conditions affecting large proportions of the population, to the vasculitides, rare syndromes leading to fast and irreversible organ failure. Atherosclerosis progresses over decades, inevitably proceeding through multiple phases of disease and causes its major complications when the vessel wall lesion ruptures, giving rise to lumen-occlusive atherothrombosis. Vasculitides of medium and large arteries progress rapidly, causing tissue ischemia through lumen-occlusive intimal hyperplasia. In both disease entities, macrophages play a decisive role in pathogenesis, but function in the context of other immune cells that direct their differentiation and their functional commitments. In atherosclerosis, macrophages are involved in the removal of lipids and tissue debris and make a critical contribution to tissue damage and wall remodeling. In several of the vasculitides, macrophages contribute to granuloma formation, a microstructural platform optimizing macrophage-T-cell interactions, antigen containment and inflammatory amplification. By virtue of their versatility and plasticity, macrophages are able to promote a series of pathogenic functions, ranging from the release of cytokines and enzymes, the production of reactive oxygen species, presentation of antigen and secretion of tissue remodeling factors. However, as short-lived cells that lack memory, macrophages are also amendable to reprogramming, making them promising targets for anti-inflammatory interventions.
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Cites
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“Meanwhile, M2-derived cytokines such as TGF-b and IL-10 are considered to have anti-inflammatory effects by inhibiting inflammatory cell recruitment and suppressing the feed-forward loops of proinflammatory cytokine production, respectively [11,36,77].”
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Macrophage plasticity and polarization: in vivo veritas
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The M1 and M2 paradigm of macrophage activation: Time for reassessment
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Getting to the site of inflammation: the leukocyte adhesion cascade updated
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Macrophages in atherosclerosis: a dynamic balance
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Macrophage-specific PPARγ controls alternative activation and improves insulin resistance
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Cited by
The glycolytic enzyme PKM2 bridges metabolic and inflammatory dysfunction in coronary artery disease
Shirai, T., Nazarewicz, R. R., Wallis, B. B., Yanes, R. E., Watanabe, R., Hilhorst, M., Tian, L., Harrison, D. G., Giacomini, J. C., Assimes, T. L., et al. (2016) · Journal of Experimental Medicine · doi:10.1084/jem.20150900 · Cited by 543
Self-citationPerivascular adipose tissue inflammation in vascular disease
Nosalski, R., & Guzik, T. J. (2017) · British Journal of Pharmacology · doi:10.1111/bph.13705 · Cited by 398
Metadata
- Authors
- Shirai, T., Hilhorst, M., Harrison, D. G., Goronzy, J. J., & Weyand, C. M.
- Venue
- Autoimmunity
- Publisher
- Informa UK Limited
- Published
- 2015-03-26
- Volume
- 48
- Issue
- 3
- Pages
- 139-151
- ISSN
- 0891-6934 (ISSN-L)
- 1607-842X
- OpenAlex
- W2084803578
- Cited by
- 160
- References
- 20
- FWCI
- 6.32
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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