miR-379-3p inhibits fat grafting survival and angiogenesis by targeting SOCS1-mediated adipose inflammation

Graphical abstract

miR-379-3p inhibits fat grafting survival and angiogenesis by targeting SOCS1-mediated adipose inflammation
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Keywords

Adipocytes
Adipose inflammation
Angiogenesis
Fat grafting
Inflammation
miR-379-3p
miRNA/mRNA pathways
Oxidative stress
Suppressor of cytokine signaling1 (SOCS1)
Survival rate

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How to Cite

1.
Zhu J, Zhao F, Han X, Li F. miR-379-3p inhibits fat grafting survival and angiogenesis by targeting SOCS1-mediated adipose inflammation. Electron. J. Biotechnol. [Internet]. 2024 Apr. 17 [cited 2024 Nov. 13];67:34-41. Available from: https://www.ejbiotechnology.info/index.php/ejbiotechnology/article/view/2023.11.001

Abstract

Background: This research probed the relevant mechanism of miR-379-3p by regulating suppressor of cytokine signaling1 (SOCS1) in the processes of inflammation, oxidative stress, and angiogenesis in fat grafting. An increasing body of research indicates the involvement of miRNA/mRNA pathways in the process of fat transplantation, yet the underlying molecular mechanisms remain to be fully elucidated.

Results: miR-379-3p knockdown improved the survival rate of adipocytes, promoted adipose tissue angiogenesis, and reduced inflammation and oxidative stress levels. miR-379-3p targeted SOCS1. SOCS1 upregulation improved adipose tissue survival and angiogenesis and reduced inflammation. miR-379-3p affected adipose tissue survival, angiogenesis, and inflammation by targeting SOCS1 expression.

Conclusions: miR-379-3p inhibits fat grafting survival and angiogenesis by targeting SOCS1 to mediate adipose inflammation, suffering a novel way to improve fat grafting technique development.

https://doi.org/10.1016/j.ejbt.2023.11.001
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References

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