MiR-3606-3p Alleviates Skin Fibrosis by Suppressing Integrin/FAK, p-AKT/p-ERK, and TGF-β Signaling Cascades

    November 2024 in “ Journal of Advanced Research ”
    Y Chen, Yiyi Gong, Mengkun Shi, Haoxing Zhu, Yulong Tang, Delin Huang, Wei Wang, Chenyi Shi, Xueyi Xia, Ying Zhang, Jian-Lan Liu, Jia Huang, Mengguo Liu, Huyan Chen, Yanyun Ma, Ziyu Wang, Lei Wang, Wenzhen Tu, Yinhuan Zhao, Jinran Lin, Jin Li, Jörg H. W. Distler, Wenyu Wu, Jiucun Wang, Xiangguang Shi
    TLDR miR-3606-3p reduces skin fibrosis by blocking key signaling pathways.
    The study investigates the role of miR-3606-3p in skin fibrosis, revealing that it is downregulated in conditions like systemic sclerosis and keloids, and its levels negatively correlate with disease severity. MiR-3606-3p targets the 3'-UTRs of ITGAV, GAB1, and TGFBR2, which are upregulated in skin fibrosis, thereby inhibiting fibrogenesis, migration, inflammation, and proliferation of fibroblasts. It achieves this by suppressing the integrin/FAK, p-AKT/p-ERK, and TGF-β signaling pathways. In vivo experiments in mice demonstrate that miR-3606-3p significantly reduces skin fibrosis, highlighting its potential as a therapeutic agent for treating skin fibrosis.
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