Gene polymorphisms of SIRT1 in patients with rheumatoid arthritis

Zhou, Jie; He, Yonglin; Fu, Lu; Lan, You‐Yu; Liu, Xiaoyan; Wu, Qian; Xu, Wang‐Dong; Huang, An‐Fang

doi:10.1111/1756-185x.14257

Cited by 14 publications

(9 citation statements)

References 37 publications

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“…Similarly, resveratrol improved arthritis scores and reduced incidence in the CIA model—both in preventive and therapeutic mode—by inhibiting Th17 and B cell function 63 . Furthermore, a recent study also identified gene polymorphisms of SIRT1 in RA patients 64 .…”

Section: Discussionmentioning

confidence: 96%

Multi-omics profiling of collagen-induced arthritis mouse model reveals early metabolic dysregulation via SIRT1 axis

Freitag

Asbrand

et al. 2022

Sci Rep

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Rheumatoid arthritis (RA) is characterized by joint infiltration of immune cells and synovial inflammation which leads to progressive disability. Current treatments improve the disease outcome, but the unmet medical need is still high. New discoveries over the last decade have revealed the major impact of cellular metabolism on immune cell functions. So far, a comprehensive understanding of metabolic changes during disease development, especially in the diseased microenvironment, is still limited. Therefore, we studied the longitudinal metabolic changes during the development of murine arthritis by integrating metabolomics and transcriptomics data. We identified an early change in macrophage pathways which was accompanied by oxidative stress, a drop in NAD+ level and induction of glucose transporters. We discovered inhibition of SIRT1, a NAD-dependent histone deacetylase and confirmed its dysregulation in human macrophages and synovial tissues of RA patients. Mining this database should enable the discovery of novel metabolic targets and therapy opportunities in RA.

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Section: Discussionmentioning

confidence: 96%

Multi-omics profiling of collagen-induced arthritis mouse model reveals early metabolic dysregulation via SIRT1 axis

Freitag

Asbrand

et al. 2022

Sci Rep

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“…However, several points need to be further discussed in the future. First, it is accepted that genetic mutation may affect mRNA expression of a gene, which will then change protein expression ( 225 , 226 ). Therefore, IL-27 gene polymorphisms may indeed change the mRNA and protein expression of IL-27, which is involved in the pathogenesis of different autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

An updated advancement of bifunctional IL-27 in inflammatory autoimmune diseases

Xu,

Wang,

Zhao

et al. 2024

Front. Immunol.

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Interleukin-27 (IL-27) is a member of the IL-12 family. The gene encoding IL-27 is located at chromosome 16p11. IL-27 is considered as a heterodimeric cytokine, which consists of Epstein–Barr virus (EBV)-induced gene 3 (Ebi3) and IL-27p28. Based on the function of IL-27, it binds to receptor IL-27rα or gp130 and then regulates downstream cascade. To date, findings show that the expression of IL-27 is abnormal in different inflammatory autoimmune diseases (including systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, Behcet’s disease, inflammatory bowel disease, multiple sclerosis, systemic sclerosis, type 1 diabetes, Vogt–Koyanagi–Harada, and ankylosing spondylitis). Moreover, in vivo and in vitro studies demonstrated that IL-27 is significantly in3volved in the development of these diseases by regulating innate and adaptive immune responses, playing either an anti-inflammatory or a pro-inflammatory role. In this review, we comprehensively summarized information about IL-27 and autoimmunity based on available evidence. It is hoped that targeting IL-27 will hold great promise in the treatment of inflammatory autoimmune disorders in the future.

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“…SIRT1 expression in the joint tissues of RA patients is obviously higher than that of general healthy population, and this abnormality positively correlates to RA severity. 28 , 29 As such, whether SIRT1 deficiency is common under RA conditions needs to be further validated. Successfully answering this question is important for the development of SIRT1-targeting anti-rheumatic therapies.…”

Section: Discussionmentioning

confidence: 99%

AMPK/SIRT1 Deficiency Drives Adjuvant-Induced Arthritis in Rats by Promoting Glycolysis-Mediated Monocytes Inflammatory Polarization

Wang¹,

He²,

Wu³

et al. 2022

JIR

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Background Exact roles of many metabolic regulators in rheumatoid arthritis (RA) are to be clarified. This study aimed to further characterize the impacts of silent information regulator 1 (SIRT1) status changes on this disease. Methods Fluctuation pattern of SIRT1 expression in adjuvant-induced arthritis (AIA) rats was monitored using periodically collected white blood cells. Another bath of AIA rats were treated by SIRT1 agonist resveratrol. Blood from these rats was used to separate monocytes and plasma, which were subjected to polymerase chain reaction (PCR), enzyme linked immunosorbent assay (ELISA), and biochemical analyses. Clinical implication of SIRT1 activation was verified by treating AIA rat monocytes with SIRT1 agonist and overexpression vector in vitro. Results SIRT1 deficiency occurred in AIA rats, which was accompanied with down-regulation of interleukin 10 (IL-10) and arginase-1 (ARG-1). Resveratrol eased oxidative stress and increased IL-10 production in vivo. Results of ELISA analysis demonstrated that resveratrol attenuated AIA severity in rats. Furthermore, it restored the altered levels of triglyceride, lactate and pyruvate in blood. Resveratrol promoted IL-10 production, and suppressed glycolysis of AIA monocytes cultured in vitro. SIRT1 overexpression similarly reshaped differentiation profile of AIA monocytes, evidenced by changes in metabolism indicators, IL-10 production and AMP-activated protein kinase (AMPK) pathway status. Although overexpressing SIRT1 in normal cells did not affect glycolysis significantly, it attenuated AMPK antagonist-caused abnormality. Conclusion SIRT1 deficiency is implicated in AIA-related immune abnormality and metabolism alteration. Activating this signaling with resveratrol would impair the inflammatory polarization of monocytes, and consequently ease the severity of RA.

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Gene polymorphisms of SIRT1 in patients with rheumatoid arthritis

Cited by 14 publications

References 37 publications

Multi-omics profiling of collagen-induced arthritis mouse model reveals early metabolic dysregulation via SIRT1 axis

Multi-omics profiling of collagen-induced arthritis mouse model reveals early metabolic dysregulation via SIRT1 axis

An updated advancement of bifunctional IL-27 in inflammatory autoimmune diseases

AMPK/SIRT1 Deficiency Drives Adjuvant-Induced Arthritis in Rats by Promoting Glycolysis-Mediated Monocytes Inflammatory Polarization

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