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Atherosclerosis in Rheumatoid Arthritis: Promoters and Opponents
Federico Carbone1, Aldo Bonaventura1, Luca Liberale1,2
1First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy.
Insights
Rheumatoid arthritis (RA) patients face higher cardiovascular disease (CVD) mortality due to accelerated atherosclerosis. Current risk assessments underestimate this risk, highlighting the need for tailored prevention strategies.
Area of Science:
- Rheumatology
- Cardiology
- Immunology
Background:
- Cardiovascular diseases (CVD) are a leading cause of mortality in rheumatoid arthritis (RA) patients.
- Current CVD risk stratification algorithms underestimate risk in RA patients.
- Accelerated atherosclerosis, sharing pathways with RA synovitis, drives acute CV events in RA.
Purpose of the Study:
- To review the pathophysiology of atherogenesis in RA patients.
- To explore potential anti-atherosclerotic effects of disease-modifying anti-rheumatic drugs (DMARDs).
Main Methods:
- Narrative review of epidemiological data and pathophysiological studies.
- Analysis of shared pathways between atherosclerosis and RA synovitis.
- Consideration of genetic, metabolic, microbiome, and inflammatory factors.
Main Results:
- RA is associated with accelerated atherosclerosis due to shared inflammatory pathways.
- Factors like genetics, metabolism, gut microbiome, and systemic inflammation contribute to atherosclerosis in RA.
- DMARDs may offer potential anti-atherosclerotic benefits.
Conclusions:
- Understanding shared pathophysiological pathways is crucial for effective CV prevention in RA.
- Tailored CV risk screening and intensive prevention strategies are needed for RA patients.
- Further research into DMARDs' anti-atherosclerotic effects is warranted.
Abstract:
Substantial epidemiological data identified cardiovascular (CV) diseases as a main cause of mortality in patients with rheumatoid arthritis (RA). In light of this, RA patients may benefit from additional CV risk screening and more intensive prevention strategies. Nevertheless, current algorithms for CV risk stratification still remain tailored on general population and are burdened by a significant underestimation of CV risk in RA patients. Acute CV events in patients with RA are largely related to an accelerated atherosclerosis. As pathophysiological features of atherosclerosis overlap those occurring in the inflamed RA synovium, the understanding of those common pathways represents an urgent need and a leading challenge for CV prevention in patients with RA. Genetic background, metabolic status, gut microbiome, and systemic inflammation have been also suggested as additional key pro-atherosclerotic factors. The aim of this narrative review is to update the current knowledge about pathophysiology of atherogenesis in RA patients and potential anti-atherosclerotic effects of disease-modifying anti-rheumatic drugs.
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