The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Anti-Inflammatory Mechanisms in the Vascular Wall
Abstract
Abstract —The role of vascular cells during inflammation is critical and is of particular importance in inflammatory diseases, including atherosclerosis, ischemia/reperfusion, and septic shock. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli. Most of the vascular inflammatory responses are mediated through the IκB/nuclear factor-κB system. Much recent work shows that vascular inflammation can be limited by anti-inflammatory counteregulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. The anti-inflammatory mechanisms in the vascular wall involve anti-inflammatory external signals and intracellular mediators. The anti-inflammatory external signals include the anti-inflammatory cytokines, transforming growth factor-β, interleukin-10 and interleukin-1 receptor antagonist, HDL, as well as some angiogenic and growth factors. Physiological laminar shear stress is of particular importance in protecting endothelial cells against inflammatory activation. Its effects are partly mediated through NO production. Finally, endogenous cytoprotective genes or nuclear receptors, such as the peroxisome proliferator–activated receptors, can be expressed by vascular cells in response to proinflammatory stimuli to limit the inflammatory process and the injury.
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Cites
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Cited by
Nitric Oxide and Peroxynitrite in Health and Disease
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The anti-inflammatory effects of exercise training in patients with type 2 diabetes mellitus
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Metadata
- Authors
- Tedgui, A., & Mallat, Z.
- Venue
- Circulation Research
- Published
- 2001-05-11
- Volume
- 88
- Issue
- 9
- Pages
- 877-887
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2140760627
- Cited by
- 422
- References
- 11
- FWCI
- 14.55
- Type
- journal article
- Language
- en
- Open access
- closed
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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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