Nano-Immunomodulators for Directing Macrophage Fate to Enhance Peripheral Nerve Repair: Advances, Challenges, and Translational Perspectives
Peripheral nerve injury remains a major clinical challenge due to inefficient axonal regeneration and limited therapeutic options. As central regulators of the repair process, macrophages dynamically transition from a pro-inflammatory to a pro-regenerative phenotype, coordinating debris clearance, axonal regrowth, remyelination, and functional restoration. However, disruptions in macrophage polarization-particularly in aging or chronic injury contexts-compromise regenerative outcomes. Here, we present a comprehensive overview of nano-immunomodulatory strategies designed to precisely direct macrophage fate for targeted peripheral nerve repair. Engineered organic, inorganic, and topography-guided nanoparticles provide spatiotemporal control of macrophage behavior via surface modifications and responsive designs, enabling phenotype reprogramming, microenvironment remodeling, and synergistic interactions with Schwann cells and regenerating axons. To present a balanced perspective, we also highlight key translational barriers-including long-term biocompatibility, immune safety, large-scale manufacturing, and regulatory challenges-that currently limit clinical application. This review highlights nano-immunomodulation as a promising approach for modulating immune-neural interfaces, offering a path toward precision therapies for peripheral nerve injury.
Authors
- Shaoyan Shi (ORCID: https://orcid.org/0000-0003-4584-2108)
- Xuehai Ou
- Qian Wang (ORCID: https://orcid.org/0000-0002-6514-3470)
- Xing Yu (ORCID: https://orcid.org/0000-0002-7917-2205)
- Dong Hu
Institutions
- Xi'an Honghui Hospital (CN)
- Xi'an Medical University (CN)
- Xi'an Jiaotong University (CN)
Publication Details
- Journal
- International Journal of Nanomedicine
- Published
- 2026-01-01
- DOI
- https://doi.org/10.2147/ijn.s558908
- Primary Topic
- Nerve injury and regeneration
- Type
- article
- Field-Weighted Citation Impact
- 0.00