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2000
Volume 25, Issue 8
  • ISSN: 1566-5240
  • E-ISSN: 1875-5666

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 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.

© 2025 Bentham Science Publishers
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miR-144/451: A Regulatory Role in Inflammation
Current Molecular Medicine 25, 948 (2025); https://doi.org/10.2174/0115665240327822241104060015
/content/journals/cmm/10.2174/0115665240327822241104060015
/content/journals/cmm/10.2174/0115665240327822241104060015
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  • Article Type:     Review Article
Keyword(s): dendritic cell; endothelial cell; epithelial cell; macrophage; miR-144/451; neutrophil; T lymphocyte

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