A tale of two diseases: atherosclerosis and rheumatoid arthritis.
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Summary
The study of the molecular mechanisms of rheumatoid arthritis may give valuable hints for research on the inflammatory/immunological mechanisms of atherosclerosis and acute coronary syndromes.
- Type
- letter
- Published
- 1999-11-23
- Cited by
- 435
- References
- 23
- Access
- Open access
- OpenAlex
- https://openalex.org/W2090560337
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:5950738
Keywords
Medicine, Intensive care medicine
References
- Atherosclerosis--an inflammatory disease.
- Perturbation of the T-cell repertoire in patients with unstable angina.
- Costimulatory molecules in human atherosclerotic plaques: an indication of antigen specific T lymphocyte activation.
- Starving the synovium: angiogenesis and inflammation in rheumatoid arthritis.
- CD4+ CD7- CD28- T cells are expanded in rheumatoid arthritis and are characterized by autoreactivity.
- Role of inflammation in coronary plaque disruption.
- Immune system activation follows inflammation in unstable angina: pathogenetic implications.
- Functional diversity of helper T lymphocytes
- Technetium stannous pyrophosphate myocardial scintigrams in patients with chest pain of varying etiology.
- Molecular bases of the acute coronary syndromes.
- Systemic inflammatory responses in acute coronary syndrome: increased activity observed in polymorphonuclear leukocytes but not T lymphocytes.
- Clinical and angiographic correlates of leukocyte activation in unstable angina.
- T lymphocyte activation in stable angina pectoris and after percutaneous transluminal coronary angioplasty.
- Acute T-cell activation is detectable in unstable angina.
- P- and E-selectin mediate recruitment of T-helper-1 but not T-helper-2 cells into inflamed tissues
- IFN-gamma potentiates atherosclerosis in ApoE knock-out mice.
- Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology.
- CD28/B7 system of T cell costimulation.
- Angiogenesis inhibitors endostatin or TNP-470 reduce intimal neovascularization and plaque growth in apolipoprotein E-deficient mice.
- Recent activation of the plaque immune response in coronary lesions underlying acute coronary syndromes
Cited by
- Reciprocal activation of leukocyte-endothelial adhesion molecules in acute coronary syndromes.
- Modulation of CD4+CD28null T Lymphocytes by Tumor Necrosis Factor-&agr; Blockade in Patients With Unstable Angina
- Overview of vasculitis and vasculopathy in rheumatoid arthritis—something to think about
- Targeting Inflammation: Impact on Atherothrombosis
- Accelerated transformation of macrophage-derived foam cells in the presence of collagen-induced arthritis mice serum is associated with dyslipidemia
- Incidence and risk of fatal myocardial infarction and stroke events in rheumatoid arthritis patients. A systematic review of the literature.
- Rheumatoide Arthritis, Inflammation und Atherosklerose
- An open-label, randomized, crossover study to assess anti-inflammatory effect of Simvastatin in Rheumatoid Arthritis statin-naïve patients with associated risk factors for cardiovascular disease
- Statin therapy in rheumatoid arthritis.
- Long-Term Anti-TNF-α Treatments Reverse the Endothelial Dysfunction in Rheumatoid Arthritis: The Biological Coherence between Synovial and Endothelial Inflammation
- Oxidative stress in patients with rheumatoid arthritis.
- Left ventricular systolic dysfunction in rheumatoid disease: an unrecognized burden?
- Public health applications of cardiovascular genomics
- Effects of C-reactive protein on K(+) channel interaction protein 2 in cardiomyocytes.
- Does anti-tnf therapy cause any change in platelet activation in ankylosing spondylitis patients?
- Fisiopatología de los síndromes coronarios agudos. Tres paradigmas para un nuevo dogma
- Active but transient improvement of endothelial function in rheumatoid arthritis patients undergoing long-term treatment with anti-tumor necrosis factor alpha antibody.
- Endothelial Dysfunction in Rheumatoid Arthritis is Improved by Anti-Tumor Necrosis Factorα Treatment
- Endothelial dysfunction in normal and abnormal glucose metabolism.
- Pathogenesis of cardiovascular disease in the presence and absence of rheumatoid arthritis
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