Cited by 164Atherosclerosis and Cardiovascular DiseasesLipoproteins and Cardiovascular HealthNitric Oxide and Endothelin Effects

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

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Welsh, Paul, Grassia, Gianluca, Botha, Shani, Sattar, Naveed, Maffia, Pasquale·2017·British Journal of Pharmacology

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.

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  • Physical activity could inhibit inflammation by reducing interleukin-6 and tumor necrosis factor-α, which could lead to atherosclerosis and elevated blood pressure.

    “PA could inhibit inflammation by inducing significant reductions in interleukin-6 and tumor necrosis factor-α, which could lead to atherosclerosis and elevated blood pressure.48”

    From Accelerometer-measured physical activity, sedentary behavior, and incidence of macrovascular and microvascular events in individuals with type 2 diabetes mellitus and prediabetes (2025) · cites this paper as [48]

    The ‘TNF-α and IL-6 in CVD > Experimental data’ section links these cytokines to inflammation and atherosclerosis, although it describes mixed effects for IL-6. The paper does not report that physical activity significantly reduces either cytokine or that these cytokines cause elevated blood pressure; searches for exercise, physical activity, and blood pressure found no such passage. Page numbers are unavailable in our copy. (LLM, conf=0.85)

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Authors
Welsh, P., Grassia, G., Botha, S., Sattar, N., & Maffia, P.
Affiliations
  • University of Glasgow (GB)
  • Hypertension in Africa Research Team (HART) North‐West University, Potchefstroom campus South Africa
  • University of Naples Federico II (IT)
Corresponding author
  • Welsh, Paul
  • Maffia, Pasquale
Venue
British Journal of Pharmacology
Publisher
Wiley
Published
2017-06-10
Volume
174
Issue
22
Pages
3898-3913
ISSN
  • 0007-1188 (ISSN-L)
  • 1476-5381
OpenAlex
W2607189590
Cited by
164
References
178
Citations by year
2026: 2 · 2025: 11 · 2024: 12 · 2023: 14 · 2022: 20 · 2021: 18 · 2020: 25 · 2019: 39 · 2018: 21 · 2017: 2
FWCI
2.42
Type
journal article
Language
en
Open access
Locations
  • British Journal of Pharmacology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
Funders
  • H2020 Marie Skłodowska-Curie Actions (Individual Fellowships 661369)
  • British Heart Foundation (PG/12/81/29897, RE/13/5/30177)
  • Engineering and Physical Sciences Research Council (EP/L014165/1)
  • European Cooperation in Science and Technology (COST Action BM1404 Mye‐EUNITER)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
vascular inflammation, atherosclerosis, cardiovascular risk, anti-inflammatory therapy, immune-inflammatory response, therapeutic target
MeSH terms
Animals, Anti-Inflammatory Agents, Anticholesteremic Agents, Antioxidants, Biological Products, Cardiovascular Diseases, Humans, Inflammation, Risk, Vitamins, Cytokines, Phospholipases A2

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