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Rheumatoid arthritis: links with cardiovascular disease and the receptor for advanced glycation end products
Lisa Carroll1, Suad Hannawi, Thomas Marwick
1Centre for Immunology and Cancer Research, Princess Alexandra Hospital, University of Queensland, Brisbane, Queensland, Australia.
Insights
Cardiovascular disease risk is elevated in rheumatoid arthritis (RA) patients due to chronic inflammation. This review explores the role of the receptor for advanced glycation end products (RAGE) and its Glycine 82 Serine polymorphism in RA-associated vascular disease.
Area of Science:
- Rheumatology
- Cardiology
- Immunology
Background:
- Cardiovascular disease risk is significantly higher in patients with chronic inflammatory conditions like rheumatoid arthritis (RA).
- Atherosclerosis shares pathophysiological similarities with autoimmune diseases, prompting a re-evaluation of cardiovascular risk in RA.
- The management of RA is evolving with targeted biological agents, necessitating a deeper understanding of associated vascular complications.
Purpose of the Study:
- To review the causes of increased vascular disease in rheumatoid arthritis.
- To explore the role of the receptor for advanced glycation end products (RAGE) in cardiovascular disease and RA.
- To discuss the potential impact of RAGE functional polymorphisms, specifically the Glycine 82 Serine variant, on disease expression.
Main Methods:
- Literature review focusing on cardiovascular risk factors in RA.
- Examination of pathophysiological mechanisms linking inflammation and vascular disease.
- Analysis of the role of RAGE and its polymorphisms in RA and cardiovascular outcomes.
Main Results:
- Chronic inflammation in RA contributes to increased cardiovascular disease risk.
- RAGE is implicated as a molecule influencing inflammation and autoimmunity, with a potential role in RA-associated vascular disease.
- Functional polymorphisms in RAGE, such as Glycine 82 Serine, may modulate disease expression.
Conclusions:
- Understanding the mechanisms linking RA and cardiovascular disease is crucial for improved patient management.
- RAGE and its genetic variants represent potential therapeutic targets or biomarkers for cardiovascular risk in RA patients.
- Further research into RAGE's role could lead to novel strategies for preventing and treating vascular complications in rheumatoid arthritis.
Abstract:
Cardiovascular (CV) disease is increased in patients with chronic inflammatory disease, including rheumatoid arthritis (RA). Furthermore it has become clear at a pathophysiological level, that atherosclerosis has striking similarities with autoimmune disease. This realization has come at a time of paradigm shift in how rheumatologists manage RA, with the availability of biological agents targeting key inflammatory cytokines. This review will focus on the possible causes of increased vascular disease in RA, including the role of traditional CV risk factors. Mechanisms potentially at play, such as C-reactive protein (CRP), altered coagulation, and cyclooxygenase (COX)-2 inhibitors will be covered in brief. The receptor for advanced glycation end products (RAGE) has been identified as a candidate molecule influencing response to ongoing inflammation and autoimmunity. There will be a focus on the role of RAGE in CV disease and RA. As has been the case with many novel molecules, functional polymorphisms are thought to alter disease expression and assist us in coming to terms with the biological activities of the parent molecule. The review will conclude with a discussion of the potential role of the RAGE Glycine 82 Serine polymorphism.
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