Published online Aug 20, 2015. doi: 10.5493/wjem.v5.i3.154
Peer-review started: March 18, 2015
First decision: April 10, 2015
Revised: April 21, 2015
Accepted: May 7, 2015
Article in press: May 8, 2015
Published online: August 20, 2015
Atherosclerosis is a chronic inflammatory disorder of the vasculature and is the primary cause of cardiovascular disease (CVD). CVD is currently the world’s leading cause of death and the numbers are predicted to rise further because of a global increase in risk factors such as diabetes and obesity. Current therapies such as statins have had a major impact in reducing mortality from CVD. However, there is a marked residual CVD risk in patients on statin therapy. It is therefore important to understand the molecular basis of this disease in detail and to develop alternative novel therapeutics. Interferon-γ (IFN-γ) is a pro-inflammatory cytokine that is often regarded as a master regulator of atherosclerosis development. IFN-γ is able to influence several key steps during atherosclerosis development, including pro-inflammatory gene expression, the recruitment of monocytes from the blood to the activated arterial endothelium and plaque stability. This central role of IFN-γ makes it a promising therapeutic target. The purpose of this editorial is to describe the key role IFN-γ plays during atherosclerosis development, as well as discuss potential strategies to target it therapeutically.
Core tip: Atherosclerosis is an inflammatory disorder of the vasculature and studies in mouse model systems have highlighted the beneficial effects of counteracting inflammation in limiting the progression of this disease. Due to its key role in inflammation and atherosclerosis development, interferon-γ (IFN-γ) is seen as a promising therapeutic target. In this editorial we discuss the role of IFN-γ in atherosclerosis together with potential therapeutic approaches against this cytokine and its key downstream targets.