Role of cytokines in cardiovascular diseases: a focus on endothelial responses to inflammation
Abstract
Complex cellular and inflammatory interactions are involved in the progress of vascular diseases. Endothelial cells, upon exposure to cytokines, undergo profound alterations of function that involve gene expression and de novo protein synthesis. The functional reprogramming of endothelial cells by cytokines is of importance especially in patients with chronic vascular inflammation. The intercellular network of dendritic cells, T-lymphocytes, macrophages and smooth muscle cells generates a variety of stimulatory cytokines [e.g. TNF-α (tumour necrosis factor-α), IL (interleukin)-1, IL-6 and IFN-γ (interferon-γ)] and growth factors that promote the development of functional and structural vascular changes. High concentrations of proinflammatory cytokines increase oxidative stress, down-regulate eNOS (endothelial nitric oxide synthase) bioactivity and induce endothelial cell apoptosis. Chemoattractant cytokines [e.g. VEGF (vascular endothelial growth factor), TGF-β1 (transforming growth factor-β1) and IL-8] are important regulators of inflammation-induced angiogenesis and are directly modulated by nitric oxide. This review will focus on the vascular mechanisms orchestrated by cytokines and summarizes the current knowledge concerning the contribution of cytokines to cardiovascular diseases.
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Proinflammatory stimuli significantly influence endothelial cell damage and apoptosis.
“This is because proinflammatory stimuli significantly influence endothelial cell damage and apoptosis [81].”
From Effect of non-surgical periodontal therapy on risk markers of cardiovascular disease: a systematic review and meta-analysis (2024) · cites this paper as [81]
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“This is because proinflammatory stimuli significantly influence endothelial cell damage and apoptosis [81].”
Background
- Authors
- KOFLER, S., NICKEL, T., & WEIS, M.
- Affiliations
- Ludwig-Maximilians-Universität München (DE)
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2005-02-18
- Volume
- 108
- Issue
- 3
- Pages
- 205-213
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- OpenAlex
- W2074639523
- Cited by
- 353
- References
- 7
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 15 · 2023: 15 · 2022: 18 · 2021: 12 · 2020: 28 · 2019: 7 · 2018: 20 · 2017: 27 · 2016: 13 · 2015: 9 · 2014: 13 · 2013: 11 · 2012: 13
- FWCI
- 3.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- cytokines, cardiovascular disease, endothelial cells, vascular inflammation, endothelial dysfunction, TNF-α, interleukin-1, interleukin-6, interferon-gamma, oxidative stress, endothelial nitric oxide synthase, endothelial cell apoptosis, angiogenesis, vascular endothelial growth factor, TGF-β1, interleukin-8, nitric oxide
- MeSH terms
- Cardiovascular Diseases, Endothelium, Vascular, Humans, Inflammation, Cytokines, Endothelial Cells
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