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

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.

How to cite: Zhu J, Zhao F, Han X, et al. miR-379-3p inhibits fat grafting survival and angiogenesis by targeting SOCS1-mediated adipose inflammation. Electron J Biotechnol 2024:67. https://doi.org/10.1016/j.ejbt.2023.11.001.