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Published on: May 6, 2014
Shared inflammatory pathways of rheumatoid arthritis and atherosclerotic cardiovascular disease
Brittany N Weber1, Jon T Giles2, Katherine P Liao3,4
1Division of Cardiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Insights
Targeting inflammation pathways like IL-6 can reduce cardiovascular disease risk in rheumatoid arthritis (RA) patients and the general population. This review examines key inflammatory pathways and their cardiovascular implications.
Area of Science:
- Rheumatology
- Cardiology
- Immunology
Background:
- Chronic inflammation is a known risk factor for cardiovascular disease (CVD) in rheumatoid arthritis (RA) and the general population.
- Targeted therapies for RA offer insights into how inhibiting specific inflammatory pathways affects cardiovascular risk.
Purpose of the Study:
- To review pro-inflammatory pathways targeted in RA therapies.
- To examine the role of these pathways in RA pathogenesis and atherosclerotic cardiovascular disease (ASCVD).
- To assess the impact of inhibiting these pathways on cardiovascular risk.
Main Methods:
- Review of existing RA therapies targeting specific pro-inflammatory pathways.
- Analysis of mechanistic data from the general population regarding these pathways and CVD.
- Focus on Interleukin-1 (IL-1), Interleukin-6 (IL-6), Tumor Necrosis Factor (TNF), and Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways.
Main Results:
- Robust data support IL-1 and IL-6 inhibition in reducing cardiovascular disease risk.
- Growing evidence indicates IL-6 inhibition benefits both RA patients and the general population in lowering CVD risk.
Conclusions:
- Inhibition of IL-1 and IL-6 pathways shows promise in mitigating cardiovascular risk associated with inflammation.
- Targeting IL-6, in particular, presents a viable strategy for cardiovascular risk management in both RA and the general populace.
Abstract:
The association between chronic inflammation and increased risk of cardiovascular disease in rheumatoid arthritis (RA) is well established. In the general population, inflammation is an established independent risk factor for cardiovascular disease, and much interest is placed on controlling inflammation to reduce cardiovascular events. As inflammation encompasses numerous pathways, the development of targeted therapies in RA provides an opportunity to understand the downstream effect of inhibiting specific pathways on cardiovascular risk. Data from these studies can inform cardiovascular risk management in patients with RA, and in the general population. This Review focuses on pro-inflammatory pathways targeted by existing therapies in RA and with mechanistic data from the general population on cardiovascular risk. Specifically, the discussions include the IL-1, IL-6 and TNF pathways, as well as the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signalling pathway, and the role of these pathways in RA pathogenesis in the joint alongside the development of atherosclerotic cardiovascular disease. Overall, some robust data support inhibition of IL-1 and IL-6 in decreasing the risk of cardiovascular disease, with growing data supporting IL-6 inhibition in both patients with RA and the general population to reduce the risk of cardiovascular disease.
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