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微小RNA-144/451:在炎症中的调节作用

miR-144/451: A Regulatory Role in Inflammation.

作者信息

Zhu Jiahao, Feng Yanhua, Zhang Lingxiao, Pang Xialing, He Sheng, Fang Lei

机构信息

Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, 225009, China.

Paediatric Department, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530002, China.

出版信息

Curr Mol Med. 2024 Nov 5. doi: 10.2174/0115665240327822241104060015.

Abstract

BACKGROUND

Inflammation is the natural defense mechanism of the body in response to injury, infection, or other stimuli. Excessive or persistent inflammatory responses can lead to the development of inflammatory diseases. Therefore, elucidating the regulatory mechanisms of inflammatory cells is crucial for understanding the pathogenesis of such diseases and devising novel therapeutic approaches. Moreover, miR-144/451 plays an important role in erythroid maturity and tumour development. Herein, we have reviewed the regulatory role of miR-144/451 in inflammation.

METHODS

Papers on miR-144, miR-451, and inflammation were retrieved from PubMed and Web of Science to be analysed and summarised.

RESULTS

miR-144/451 plays a significant role in modulating inflammatory responses. Pro- and anti-inflammatory gene transcription is regulated by miR-144/451 binding to the 3' untranslated regions. Studies have shown that miR-451 inhibits the activation of various inflammatory cells, including macrophages, neutrophils, and T lymphocytes, thereby reducing the release of inflammatory mediators. However, miR-144 expression varies in different inflammatory diseases. miR-144 expression is downregulated in macrophages after induction by lipopolysaccharide, cysteine, or Mycobacterium tuberculosis, which promotes the secretion of inflammatory mediators; nonetheless, miR-144-3p overexpression in macrophages can aggravate atherosclerosis. Meanwhile, miR-144 overexpression prevents disruption of the lung endothelial cell barrier, whereas it exacerbates endothelial cell injury in Crohn's disease.

CONCLUSION

miR-144/451 may serve as a potential target for the treatment of inflammatory diseases.

摘要

背景

炎症是机体对损伤、感染或其他刺激的自然防御机制。过度或持续的炎症反应可导致炎症性疾病的发生。因此,阐明炎症细胞的调控机制对于理解此类疾病的发病机制和设计新的治疗方法至关重要。此外,miR-144/451在红细胞成熟和肿瘤发展中起重要作用。在此,我们综述了miR-144/451在炎症中的调控作用。

方法

从PubMed和Web of Science检索有关miR-144、miR-451和炎症的论文进行分析和总结。

结果

miR-144/451在调节炎症反应中起重要作用。促炎和抗炎基因转录受miR-144/451与3'非翻译区结合的调控。研究表明,miR-451抑制包括巨噬细胞、中性粒细胞和T淋巴细胞在内的各种炎症细胞的激活,从而减少炎症介质的释放。然而,miR-144在不同炎症性疾病中的表达有所不同。脂多糖、半胱氨酸或结核分枝杆菌诱导后,巨噬细胞中miR-144表达下调,这促进了炎症介质的分泌;尽管如此,巨噬细胞中miR-144-3p过表达可加重动脉粥样硬化。同时,miR-144过表达可防止肺内皮细胞屏障破坏,而在克罗恩病中则会加重内皮细胞损伤。

结论

miR-144/451可能成为炎症性疾病治疗的潜在靶点。

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