The DOI matches its Crossref record; 246 of the 246 references it cites were found in a registry or an index.
Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets
Open accessAbstract
Atherosclerosis, a chronic inflammatory disorder of the arteries, is responsible for most deaths in westernized societies with numbers increasing at a marked rate in developing countries. The disease is initiated by the activation of the endothelium by various risk factors leading to chemokine-mediated recruitment of immune cells. The uptake of modified lipoproteins by macrophages along with defective cholesterol efflux gives rise to foam cells associated with the fatty streak in the early phase of the disease. As the disease progresses, complex fibrotic plaques are produced as a result of lysis of foam cells, migration and proliferation of vascular smooth muscle cells and continued inflammatory response. Such plaques are stabilized by the extracellular matrix produced by smooth muscle cells and destabilized by matrix metalloproteinase from macrophages. Rupture of unstable plaques and subsequent thrombosis leads to clinical complications such as myocardial infarction. Cytokines are involved in all stages of atherosclerosis and have a profound influence on the pathogenesis of this disease. This review will describe our current understanding of the roles of different cytokines in atherosclerosis together with therapeutic approaches aimed at manipulating their actions.
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“Moreover, OxLDL uptake by CD36 causes expression of cytokines via a mechanism involving TLR2-TLR4 [225].”
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Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines
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Metadata
- Authors
- Ramji, D. P., & Davies, T. S.
- Venue
- Cytokine & Growth Factor Reviews
- Publisher
- Elsevier BV
- Published
- 2015-12
- Volume
- 26
- Issue
- 6
- Pages
- 673-685
- ISSN
- 1359-6101 (ISSN-L)
- OpenAlex
- W1840986526
- Cited by
- 469
- References
- 246
- FWCI
- 2.41
- Type
- journal article
- Language
- en
- Open access
- hybrid
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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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