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系统性硬化症中的代谢紊乱

Metabolic perturbations in systemic sclerosis.

作者信息

O'Reilly Steven

机构信息

Department of Biosciences, Durham University, Durham, UK.

出版信息

Curr Opin Rheumatol. 2022 Jan 1;34(1):91-94. doi: 10.1097/BOR.0000000000000824.

DOI:10.1097/BOR.0000000000000824
PMID:34636347
Abstract

PURPOSE OF REVIEW

The aim of this review is to evaluate the recent evidence of the role of metabolism in systemic sclerosis (SSc), highlighting specific aberrations and to appraise the feasibility of targeting these therapeutically.

RECENT FINDINGS

SSc is an autoimmune disease that is characterised by three facets: vascular problems, inflammation, and fibrosis. The fibrosis primarily affects the skin and lungs and currently, no antifibrotic treatment has been found effective. In recent years a renaissance in metabolism research has begun with renewed vigour in the role of metabolism in disease, particularly in the immune system. Alterations in glycolysis and utilisation of specific metabolic pathways in specific cell types have been associated with specific diseases. Most recently alterations in glycolysis and glutaminolysis have been determined in SSc fibroblasts mediating fibrosis. Reduced nicotinamide adenine dinucleotide levels have also been described in SSc.

SUMMARY

Specific metabolic aberrations have been described in SSc and this may lead to novel therapeutic targets in this disease.

摘要

综述目的

本综述旨在评估代谢在系统性硬化症(SSc)中作用的最新证据,突出特定异常情况,并评估针对这些异常进行治疗的可行性。

最新发现

SSc是一种自身免疫性疾病,其特征有三个方面:血管问题、炎症和纤维化。纤维化主要影响皮肤和肺部,目前尚未发现抗纤维化治疗有效。近年来,代谢研究再度兴起,对代谢在疾病,尤其是免疫系统中的作用重新焕发出活力。糖酵解的改变以及特定细胞类型中特定代谢途径的利用与特定疾病相关。最近在介导纤维化的SSc成纤维细胞中确定了糖酵解和谷氨酰胺分解的改变。在SSc中也描述了烟酰胺腺嘌呤二核苷酸水平降低。

总结

SSc中已描述了特定的代谢异常,这可能会为该疾病带来新的治疗靶点。

相似文献

1
Metabolic perturbations in systemic sclerosis.系统性硬化症中的代谢紊乱
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2
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Interferon regulatory factor 7 (IRF7) represents a link between inflammation and fibrosis in the pathogenesis of systemic sclerosis.干扰素调节因子 7(IRF7)在系统性硬化症的发病机制中代表了炎症和纤维化之间的联系。
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Nintedanib inhibits fibroblast activation and ameliorates fibrosis in preclinical models of systemic sclerosis.尼达尼布抑制成纤维细胞活化,并改善全身性硬皮病的临床前模型中的纤维化。
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Interleukin-13-producing CD8+ T cells mediate dermal fibrosis in patients with systemic sclerosis.产生白细胞介素-13的CD8+ T细胞介导系统性硬化症患者的皮肤纤维化。
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The -Antioxidant Response Element Signaling Pathway Controls Fibrosis and Autoimmunity in Scleroderma.抗氧化反应元件信号通路调控硬皮病的纤维化和自身免疫。
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Low RUNX3 expression alters dendritic cell function in patients with systemic sclerosis and contributes to enhanced fibrosis.RUNX3 低表达改变系统性硬化症患者树突状细胞功能,并促进纤维化增强。
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10
Systemic sclerosis.系统性硬化症。
J Dermatol. 2018 Feb;45(2):128-138. doi: 10.1111/1346-8138.14153. Epub 2017 Dec 10.

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