Interleukin-6 Signaling in Atherosclerosis: From Molecular Mechanisms To Clinical Outcomes

Author:

Papastamos Charalampos1,Antonopoulos Alexios S.1,Simantiris Spyridon2,Koumallos Nikolaos2,Sagris Marios1,Theofilis Panagiotis2,Oikonomou Evangelos3,Siasos Gerasimos3,Tsioufis Konstantinos1,Tousoulis Dimitris1

Affiliation:

1. 1st Cardiology Department, National and Kapodistrian University of Athens, Hippokration General Hospital, Athens, Greece

2. 1st Cardiology Department, National and Kapodistrian University of Athens, Hippokration General Hospital, Athens, Greece.

3. 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, Athens, Greece

Abstract

Abstract: Interleukin-6 (IL-6) is a cytokine centrally involved in several immune responses and it has been recognized as a driver of enhanced atherothrombotic risk. Immunity and inflammation are intrinsically involved in atherosclerosis progression. This generated ‘inflammation hypothesis’, which is now validated in large-scale clinical trials. Abundant evidence supports the distinctive role of IL-6 in coronary artery disease. The focus on this cytokine stems from epidemiological studies linking high plasma concentrations of IL-6 with greater risk for adverse cardiovascular events, genetic studies which implicate a causative role of IL-6 in atherosclerosis and murine data which support the involvement of IL-6 in various pathophysiological cascades of atherothrombosis. The fact that high IL-6 levels are equivalent to increased cardiovascular risk created an unmet need to address those who are at ‘residual inflammatory risk’. Moreover, the opposing effects of IL-6 underlined the importance of deciphering specific signaling cascades, which may be responsible for different effects. Finally, murine data and some small clinical trials highlighted the possibility of reversing the pro-atherogenic effects of IL-6 by directly targeting it. While IL-1 blockage was proved effective, it is reasonable to examine if moving more downstream in the inflammation cascade could be more selective and effective than other anti-inflammatory therapies. In the present review, we examine the role of IL-6 as a biomarker of ‘residual inflammatory risk’, its vital role in the pathophysiology of atherosclerosis progression and the possibility of targeting it to stall coronary artery disease progression.

Publisher

Bentham Science Publishers Ltd.

Subject

Drug Discovery,General Medicine

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