After peripheral nerve injury (PNI), there will be a vicious cycle of iron metabolism disorder and oxidative stress at the injured site: excessive ferrous ions (Fe²⁺) produce a large amount of reactive oxygen species (ROS) through the Fenton reaction, triggering mitochondrial and endoplasmic reticulum (ER) stress, while insufficient vascular remodeling severely hinders nerve regeneration. Currently, the commonly used autologous transplantation in clinical practice has problems such as donor shortage and postoperative complications, while traditional nerve conduits are difficult to regulate the complex regenerative microenvironment and have limited repair effects.

Link to the paper (DOI)：https://doi.org/10.1002/adma.202507931