GDNF receptor-expressing mesenchymal progenitor subpopulation within skeletal muscle responds to peripheral nerve injury by sensing GDNF and secreting BDNF, thereby directly promoting nerve regeneration through facilitating remyelination by Schwann cells.

Establishing transcriptional profiles of nerve-inhabitant cells as resource to foster the fundamental understanding of peripheral nerves.

In vivo and in vitro experiments confirm the conspicuous antineoplastic efficacy of NIR-III photothermal therapy under the premise of ensuring biosafety.

In reporter mice, subtypes of peripheral neurons show different regenerative capabilities after nerve injury and activate common pathways but also specific ones, indicating a different intrinsic growth response among them.

YAP and TAZ, potent concoproteins and therapeutic targets in cancer therapy, are essential for Schwann cells to support peripheral nerve regeneration.

CX3CR1-signaling in sensory ganglia macrophages mediates their proliferation/activation, as well as the production of pro-inflammatory mediators that contribute to neuropathic pain.

Myelin generation during development and nerve regeneration is guaranteed by responsive backup circuits that coordinate class IIa HDACs to repress the expression of negative regulators of myelination and permit Schwann cell differentiation in response to cAMP.

A murine model for a novel surgical concept demonstrates potential advances of neuroprosthetic interfacing.

Dynamic regulation of feedforward inhibition from parvalbumin-expressing inhibitory neurons is linked to the gradual restoration of cortical sensory processing following auditory nerve damage.

TEAD1 is a major partner transcription factor of YAP/TAZ crucial for developmental myelination and remyelination of peripheral nerves.