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
Review
. 2014 Sep;16(9):435.
doi: 10.1007/s11883-014-0435-z.

Inflammation and cardiovascular disease: from pathogenesis to therapeutic target

Affiliations
Review

Inflammation and cardiovascular disease: from pathogenesis to therapeutic target

Enrica Golia et al. Curr Atheroscler Rep. 2014 Sep.

Abstract

Atherosclerosis represents the most common pathological substrate of coronary heart disease (CHD), and the characterization of the disease as a chronic low-grade inflammatory condition is now largely accepted. A number of mediators of inflammation have been widely studied, both as surrogate biomarkers and as causal agents, in the pathophysiological network of atherogenesis and plaque vulnerability. The epidemiological observation that biomarkers of inflammation are associated with clinical cardiovascular risk supports the theory that targeted anti-inflammatory treatment appears to be a promising strategy in reducing residual cardiovascular risk on the background of traditional medical therapy. A large number of randomized controlled trials have shown that drugs commonly used in cardiovascular disease (CVD), such as statins, may be effective in the primary and secondary prevention of cardiovascular events through an anti-inflammatory effect. Moreover, several anti-inflammatory drugs are being tested for their potential to reduce residual cardiovascular risk on the background of validated medical therapy for atherosclerotic disease. In this paper, we review relevant evidence with regard to the relationship between inflammation and CVD, from pathogenesis to therapeutic strategies.

PubMed Disclaimer

References

    1. J Clin Lipidol. 2010 May-Jun;4(3):156-64 - PubMed
    1. Arterioscler Thromb Vasc Biol. 2005 May;25(5):923-31 - PubMed
    1. Circ Res. 2010 Feb 5;106(2):383-90 - PubMed
    1. Heart. 2007 Feb;93(2):244-6 - PubMed
    1. N Engl J Med. 1986 Feb 20;314(8):488-500 - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources