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

Br J Pharmacol. 2017 Nov;174(22):3898-3913. doi: 10.1111/bph.13818. Epub 2017 Jun 10.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Anticholesteremic Agents / therapeutic use
  • Antioxidants / therapeutic use
  • Biological Products / therapeutic use
  • Cardiovascular Diseases / immunology
  • Cardiovascular Diseases / metabolism
  • Cardiovascular Diseases / prevention & control*
  • Cytokines / immunology
  • Humans
  • Inflammation / drug therapy*
  • Phospholipases A2 / metabolism
  • Risk
  • Vitamins / therapeutic use

Substances

  • Anti-Inflammatory Agents
  • Anticholesteremic Agents
  • Antioxidants
  • Biological Products
  • Cytokines
  • Vitamins
  • Phospholipases A2