Visfatin (pre-B cell colony-enhancing factor) gene expression in patients with rheumatoid arthritis: Figure 1

Matsui, Hirohumi; Tsutsumi, Akito; Sugihara, Makoto; Suzuki, Takeshi; Iwanami, Keiichi; Kohno, Mika; Goto, Daisuke; Matsumoto, Isao; Ito, Satoshi; Sumida, Takayuki

doi:10.1136/ard.2007.077578

Cited by 36 publications

(29 citation statements)

References 10 publications

(9 reference statements)

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“…The authors proposed that these adipokines could coordinate the inflammatory process in RA, and at the very least could serve as biomarkers for the disease. These findings were confirmed by Nowell et al [30] Bretano et al [24] and Matsui et al [25] Nowell and colleagues detected elevated levels of Nampt in synovial fluid from RA patients when compared with osteoarthritis (OA) patients [30] Nampt expression was immunolocalized within the synovial lymphoid aggregates, which consisted of B cells, T cells, dendritic cells, and plasma cells, as well as within several additional cell types associated with the pathophysiology of RA, including endothelial cells, fibroblast-like synoviocytes (FLS), macrophage-like synoviocytes (MLS), and adipocyte-like cells [30]. Bretano et al [24] also demonstrated that Nampt expression was elevated in the joints of RA patients, especially in the FLS localized at the points of invasion into the synovial lining and cartilage.…”

Section: Epidemiological Surveys Of Nampt Expression In Rheumatoid Arsupporting

confidence: 80%

“…Bretano et al [24] also demonstrated that Nampt expression was elevated in the joints of RA patients, especially in the FLS localized at the points of invasion into the synovial lining and cartilage. Matsui et al [25] detected elevated Nampt mRNA expression in synovial tissue, peripheral blood mononuclear cells (PBMCs), and peripheral blood granulocytes (PBGs) isolated from RA patients compared to healthy controls. Subsequent surveys [17,[26][27][28][29] have verified that expression of Nampt in serum, synovial fluid, and synovial tissue is elevated in patients with RA.…”

Section: Epidemiological Surveys Of Nampt Expression In Rheumatoid Armentioning

confidence: 99%

“…Nampt expression is up-regulated in a variety of acute and chronic inflammatory diseases including acute lung injury [14], sepsis [15], inflammatory bowel disease, [16,17] atherosclerosis, [18,19] osteoarthritis [20][21][22] and rheumatoid arthritis [17,[23][24][25][26][27][28][29][30]. Recent findings have demonstrated that targeted inhibition of Nampt attenuates the inflammatory process and disease progression in mouse models of arthritis [31,32], suggesting that Nampt plays a key role in the pathogenesis of RA.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Epidemiological Surveys Of Nampt Expression In Rheumatoid Arsupporting

confidence: 80%

Section: Epidemiological Surveys Of Nampt Expression In Rheumatoid Armentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nicotinamide Phosphoribosyltransferase in Rheumatoid Arthritis

Heruth¹,

Zhang²,

Ye³

2011

JBABM /Vol.3.4 (2011)

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“…With this regard, several authors have described that the level of visfatin in serum is increased in RA patients in comparison to healthy controls [21][22][23][24][25].…”

Section: Visfatin In Rheumatoid Arthritis (Ra)mentioning

confidence: 99%

“…The synovial joint is a unique tissue where adipokines may be regulated by specific pathways [33], therefore it is of interest that visfatin expression is reportedly increased in RA human synovial tissue [22,34]. Specifically, although visfatin was expressed by endothelial cells, adipocytes, and lymphoid aggregates, it was predominantly expressed by RA synovial fibroblasts (RASF) particularly within the synovial lining and at sites of cartilage invasion [28,34,35].…”

Section: Visfatin In Rheumatoid Arthritis (Ra)mentioning

confidence: 99%

Visfatin: a new player in rheumatic diseases

Gómez

Suárez²,

Villalvilla³

et al. 2013

Immunometabolism

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During the last 50 years the number of overweight and obese people in developed countries has increased dramatically. The consequences of this excessive fat accumulation have been associated with a multitude of comorbidities, mainly related to the cardiovascular system and glucose and lipid metabolism. However, obesity also has an impact on other diseases, as an enhancer of certain pathological aspects or as a susceptibility factor, including certain rheumatic diseases such as rheumatoid arthritis (RA), osteoarthritis (OA) and systemic lupus erythematosus (SLE). The link between obesity and these rheumatic diseases has been purported to be via the action of metabolic factors produced by adipose tissue, adipokines. Among these adipokines are leptin and adiponectin, which have been extensively studied. Our knowledge of the role of other relevant newer adipokines, such as visfatin, in the arthritides is rapidly growing. Therefore, in this review our aim is to summarize the current literature regarding the association between visfatin and the most relevant rheumatic diseases.

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CNS Targets of Adipokines

Beall

Hanna

Ellacott

2017

Comprehensive Physiology

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Our understanding of adipose tissue as an endocrine organ has been transformed over the last 20 years. During this time, a number of adipocyte-derived factors or adipokines have been identified. This article will review evidence for how adipokines acting via the central nervous system (CNS) regulate normal physiology and disease pathology. The reported CNS-mediated effects of adipokines are varied and include the regulation of energy homeostasis, autonomic nervous system activity, the reproductive axis, neurodevelopment, cardiovascular function, and cognition. Due to the wealth of information available and the diversity of their known functions, the archetypal adipokines leptin and adiponectin will be focused on extensively. Other adipokines with established CNS actions will also be discussed. Due to the difficulties associated with studying CNS function on a molecular level in humans, the majority of our knowledge, and as such the studies described in this paper, comes from work in experimental animal models; however, where possible the relevant data from human studies are also highlighted. © 2017 American Physiological Society. Compr Physiol 7:1359-1406, 2017.

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Visfatin (pre-B cell colony-enhancing factor) gene expression in patients with rheumatoid arthritis: Figure 1

Cited by 36 publications

References 10 publications

Nicotinamide Phosphoribosyltransferase in Rheumatoid Arthritis

Nicotinamide Phosphoribosyltransferase in Rheumatoid Arthritis

Visfatin: a new player in rheumatic diseases

CNS Targets of Adipokines

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