Targeting inflammation to reduce cardiovascular disease risk: a realistic clinical prospect?

Abstract

Data from basic science experiments is overwhelmingly supportive of the causal role of immune-inflammatory response(s) at the core of atherosclerosis, and therefore, the theoretical potential to manipulate the inflammatory response to prevent cardiovascular events. However, extrapolation to humans requires care and we still lack definitive evidence to show that interfering in immune-inflammatory processes may safely lessen clinical atherosclerosis. In this review, we discuss key therapeutic targets in the treatment of vascular inflammation, placing basic research in a wider clinical perspective, as well as identifying outstanding questions.

Linked articles: This article is part of a themed section on Targeting Inflammation to Reduce Cardiovascular Disease Risk. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.22/issuetoc and http://onlinelibrary.wiley.com/doi/10.1111/bcp.v82.4/issuetoc.

Figure 1

Pro‐atherogenic and inflammatory pathways targeted by prospective anti‐atherosclerotic antibodies and inhibitors.

Figure 2

Summary of studies investigating the role of vitamin C in CVD risk. Data from Boekholdt et al. (2006), Ye and Song (2008) and Myung et al. (2013).