Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2013 Feb;123(2):540-1.
doi: 10.1172/JCI66843. Epub 2013 Feb 1.

Linking endothelial dysfunction with endothelial cell activation

James K Liao  1
Affiliations

Linking endothelial dysfunction with endothelial cell activation

James K Liao. J Clin Invest. 2013 Feb.

Abstract

The thin layer of cells that lines the interior of blood vessels, known as the endothelium, plays a complex role in vascular biology. The endothelium mediates blood vessel tone, hemostasis, neutrophil recruitment, hormone trafficking, and fluid filtration. Endothelial dysfunction, as defined by a lack of NO, has been linked to a variety of disease states, including atherosclerosis, diabetes mellitus, coronary artery disease, hypertension, and hypercholesterolemia. Indeed, restoration of endothelial function is one of the earliest recognizable benefits of statin therapy. In 1995, James Liao and colleagues published a study in the JCI demonstrating that NO is a vascular protective factor that limits endothelial activation and prevents leukocyte adhesion to the vessel wall.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Role of endothelial dysfunction and endothelial cell activation in vascular disease.
Cardiovascular risk factors, such as hypercholesterolemia, smoking, and oxidative stress, are important mediators of endothelial dysfunction, while proinflammatory cytokines, turbulent flow, and advanced glycation end-products (AGEs) are important mediators of endothelial cell activation via the activation of the transcription factor, NF-κB. NO from eNOS or NO donors reduces endothelial cell activation through inhibition of NF-κB. Loss of NO leads to increased endothelial cell activation. Likewise, endothelial cell activation can cause endothelial dysfunction. Both endothelial dysfunction and endothelial cell activation lead to atherosclerosis and vascular disease by increasing vasoconstriction, SMC proliferation, platelet aggregation, leukocyte adhesion, LDL oxidation, and MMP activation.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. De Caterina R, et al. Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. J Clin Invest. 1995;96(1):60–68. doi: 10.1172/JCI118074. - DOI - PMC - PubMed
    1. Gimbrone MA, Jr, Nagel T, Topper JN. Biomechanical activation: An emerging paradigm in endothelial adhesion biology. J Clin Invest. 1997;99(8):1809–1813. doi: 10.1172/JCI119346. - DOI - PMC - PubMed
    1. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002;105(9):1135–1143. doi: 10.1161/hc0902.104353. - DOI - PubMed
    1. Kubes P, Suzuki M, Granger DN. Nitric oxide: An endogenous modulator of leukocyte adhesion. Proc Natl Acad Sci U S A. 1991;88(11):4651–4655. doi: 10.1073/pnas.88.11.4651. - DOI - PMC - PubMed
    1. Baeuerle PA. Ikappab-nf-kappab structures: At the interface of inflammation control. Cell. 1998;95(6):729–731. doi: 10.1016/S0092-8674(00)81694-3. - DOI - PubMed

Publication types

MeSH terms

Substances