Publication Name	World Journal of Stem Cells
Manuscript ID	119260
Country	China

Category	Cell Biology
Manuscript Type	Basic Study
Article Title	Exosomal miR-181d-5p promotes spinal cord injury repair by driving microglial polarization from M1 to M2 phenotype
Manuscript Source	Unsolicited Manuscript
All Author List	Wei Wang, Bin Wang and Hua Yin
Funding Agency and Grant Number	Funding Agency Grant Number Basic Public Welfare Research Plan of Zhejiang Province LGF21H090015 Taizhou Science and Technology Plan 20ywa08
Corresponding Author	Hua Yin, Department of Orthopedics, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, No. 150 Ximen Road, Linhai District, Taizhou 317600, Zhejiang Province, China. yinhuacaro@126.com
Key Words	Spinal cord injury; Exosomes; miR-181d-5p; M1 phenotype; M2 phenotype; Neuroinflammation
Core Tip	Our work demonstrates that mesenchymal stem cell-exosomes promote recovery after spinal cord injury by delivering miR-181d-5p to microglia, thereby repolarizing them from an M1 to an M2 state. This proposed mechanism provides fresh insight into the therapeutic action of mesenchymal stem cell-exosomes and underscores the translational potential of miR-181d-5p in spinal cord injury treatment strategies.
Citation	Wang W, Wang B, Yin H. Exosomal miR-181d-5p promotes spinal cord injury repair by driving microglial polarization from M1 to M2 phenotype. World J Stem Cells 2026; In press

Received	2026-01-23 06:29
Peer-Review Started	2026-01-23 06:39
First Decision by Editorial Office Director	2026-02-06 09:35
Return for Revision	2026-02-06 09:35
Revised	2026-03-10 01:36
Publication Fee Transferred	2026-03-12 01:43
Second Decision by Editor	2026-04-23 02:43
Second Decision by Editor-in-Chief
Final Decision by Editorial Office Director	2026-05-07 08:05
Articles in Press	2026-05-07 08:05
Edit the Manuscript by Language Editor
Typeset the Manuscript

ISSN	1948-0210 (online)
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Copyright	©Author(s) (or their employer(s)) 2026. No commercial re-use. See Permissions. Published by Baishideng Publishing Group Inc.
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