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Cited by 285

The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.

Interleukin 8 and cardiovascular disease

Apostolakis, S., Vogiatzi, K., Amanatidou, V., Spandidos, D. A.·2009·Cardiovascular Research

Abstract

Since the establishment of the inflammatory basis of atherosclerosis, several pro- or anti-inflammatory agents have been examined as potential mediators of the biochemical pathways of lesion formation. Interleukin (IL)-8 was first characterized in 1987. Since then, knowledge regarding its role in leucocyte trafficking and activation has advanced rapidly, especially in the field of cardiovascular disease. In the scientific literature, there is sufficient evidence to support beyond any doubt the involvement of IL-8 in the establishment and preservation of the inflammatory micro-environment of the insulted vascular wall. However, how the information derived from in vitro studies and animal models can be applied in clinical practice has yet to be determined. In the present review, the available evidence regarding the role of IL-8 in cardiovascular disease is presented, and future perspectives are discussed.

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Metadata

Authors
Apostolakis, S., Vogiatzi, K., Amanatidou, V., & Spandidos, D. A.
Venue
Cardiovascular Research
Published
2009-07-18
Volume
84
Issue
3
Pages
353-360
ISSN
0008-6363 (ISSN-L)
OpenAlex
W2131918803
Cited by
285
References
58
FWCI
3.31
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Interleukin 8 and cardiovascular disease. https://app.cochat.ai/papers/10.1093/cvr/cvp241
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Apostolakis, S., Vogiatzi, K., Amanatidou, V., & Spandidos, D. A. (2009). Interleukin 8 and cardiovascular disease. Cardiovascular Research. https://doi.org/10.1093/cvr/cvp241

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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.