Pathophysiology of rheumatoid arthritis

Cooles, Faye A H; Isaacs, John D.

doi:10.1097/bor.0b013e32834518a3

Cited by 161 publications

(115 citation statements)

References 54 publications

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“…The pathophysiology of RA is complex, perpetuated by an arsenal of cells whose functions have been altered often by RA-associated genes and/or environmental triggers and converted to autoimmune cells and complexes, or made to follow an inflammatory pathway [5,6]. Prominent amongst the cytokine mediators of inflammation triggered by lymphocytic activities are tumour necrosis factor (TNF-α) and interleukins (IL-1, IL-6) [5], resulting in increasing levels of oxidative stress [7].…”

Section: Introductionmentioning

confidence: 99%

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Platelet and red blood cell interactions and their role in rheumatoid arthritis

Olumuyiwa-Akeredolu

Pretorius

2015

Rheumatol Int

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Section: Introductionmentioning

confidence: 99%

“…Prominent amongst the cytokine mediators of inflammation triggered by lymphocytic activities are tumour necrosis factor (TNF-α) and interleukins (IL-1, IL-6) [5], resulting in increasing levels of oxidative stress [7]. Lipid parameters (e.g.…”

Section: Introductionmentioning

confidence: 99%

Platelet and red blood cell interactions and their role in rheumatoid arthritis

Olumuyiwa-Akeredolu

Pretorius

2015

Rheumatol Int

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“…Although the etiology of the disease has not been fully elucidated, the pathogenesis of RA is characterized by the influx of cells from both the innate and the adaptive immune systems [3][4][5]. These infiltrating cells induce increased pro-inflammatory cytokine production, decreased synthesis of anti-inflammatory cytokines, and the subsequent activation and proliferation of synovial tissue.…”

Section: Introductionmentioning

confidence: 99%

“…These infiltrating cells induce increased pro-inflammatory cytokine production, decreased synthesis of anti-inflammatory cytokines, and the subsequent activation and proliferation of synovial tissue. The severe imbalance in the cytokine signaling pathways ultimately lead to the thickening and progressive destruction of joint membrane, cartilage and bone [2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Nicotinamide Phosphoribosyltransferase in Rheumatoid Arthritis

Heruth¹,

Zhang²,

Ye³

2011

JBABM /Vol.3.4 (2011)

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Nicotinamide Phosphoribosyltransferase (Nampt) is a pleiotropic protein with multiple functions, including catalyzing a rate-limiting reaction of nicotinamide adenine dinucleotide (NAD) synthesis in a mammalian salvage pathway and mediating the innate immune system's inflammatory response. The enzymatic activity of Nampt has been well characterized; however, the mechanism(s) by which Nampt regulates cytokine signaling have not been fully elucidated. Rheumatoid arthritis (RA) a chronic, systemic autoimmune disorder in which the pathological roles of proinflammatory cytokines such as Tumor Necrosis Factor (TNF), interleukin (IL)-1β, and IL-6 have been clearly demonstrated. Recently, studies have shown that serum and synovial levels of Nampt are elevated in both RA patients and in mice with collagen induced arthritis (CIA), and that inhibition of Nampt activity decreases the expression of TNF, IL-1β, and IL-6. Thus, Nampt may represent a potential new therapeutic target in RA. This review will focus on Nampt's role in NAD metabolism and cytokine signaling in the context of the pathophysiology and therapeutic potential of RA.

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“…The etiology of RA is unclear, but it has been suggested that the inflammatory and autoimmune activities lead to destruction of joint surfaces. This destruction restricts the joint motion and causes some deformities (1,4).…”

Section: Introductionmentioning

confidence: 99%

The Prevalence of “MEFV” Gene Mutations in Rheumatoid Arthritis Patients Inhabiting the Van Province and Surroundings

Özkol¹,

Yildirim²,

Tülüce³

et al. 2014

Turk J Phys Med Rehab

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Objective: An inhibitory protein of inflammation pyrin/marenostrin is encoded by the Mediterranean fever (MEFV) gene. Mutations of this gene are known to cause familial Mediterranean fever (FMF) disease. A relation between mutations of the MEFV gene and rheumatic diseases was also suggested. The aim of the present study was to investigate the frequency of four common mutations of the MEFV gene in 110 rheumatoid arthritis (RA) patients and 98 healthy controls (HC) inhabiting a region of eastern Turkey. Material and Methods: DNA extraction was realized by salting out method from peripheral blood lymphocytes of all subjects included in the study. Polymerase chain reactions (PCR) amplification of exon 10 was performed by the appropriate primers, and single-nucleotide polymorphisms (SNPs) were detected by specific restriction endonucleases recognizing the mutational DNA or wild-type DNA regions. Results: Mutation frequency of RA patients was higher than in HC, but this result was not statistically significant (p>0.05). Conclusion:The MEFV mutation rate of RA patients living in eastern Turkey was not significantly different from HC. Further studies are needed to investigate other gene mutations that may affect RA etiopathogenesis.

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Pathophysiology of rheumatoid arthritis

Abstract: Our knowledge of rheumatoid arthritis pathogenesis continues to expand. The last year has seen some key findings, including the identification of novel, potentially tractable targets for further therapeutic research.

Cited by 161 publications

References 54 publications

Platelet and red blood cell interactions and their role in rheumatoid arthritis

Platelet and red blood cell interactions and their role in rheumatoid arthritis

Nicotinamide Phosphoribosyltransferase in Rheumatoid Arthritis

The Prevalence of “MEFV” Gene Mutations in Rheumatoid Arthritis Patients Inhabiting the Van Province and Surroundings

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