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Peer-reviewedCC BYFrontiers in aging neuroscience

Pathological remodeling and functional evolution of the corneal nervous system in ocular surface dyshomeostasis.

  • Jiayang Liu1
  • Hanwen Lu2
  • Xiyao Liu3
  1. 1Department of Ophthalmology, First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China.
  2. 2Department of Neurosurgery and Department of Neuroscience, Fujian Key Laboratory of Brain Tumors Diagnosis and Precision Treatment, Xiamen Key Laboratory of Brain Center, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China.
  3. 3Department of Neurosurgery, First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China.
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Abstract

The corneal nerve plexus is essential to ocular surface homeostasis through sensory detection, trophic support, epithelial repair, blinking, and lacrimal reflexes. In dry eye disease (DED), chronic hyperosmolar, inflammatory, mechanical, and age-related stressors alter nerve morphology and function, contributing to reduced nerve density, aberrant regeneration, microneuroma formation, sensory loss, and peripheral or central sensitization. This review summarizes the ultrastructure of corneal innervation and the molecular basis of corneal sensory transduction, with emphasis on TRPM8, TRPV1, TRPA1, Piezo2, and acid-sensing ion channels. It then examines bidirectional neuroimmune signaling involving dendritic cells, cytokines, neuropeptides, and diminished neurotrophic support. We further discuss the relationship between age-related corneal hypoesthesia, local small-fiber degeneration, and systemic neurodegenerative disorders, while noting the limited disease specificity of currently proposed corneal biomarkers. Finally, we evaluate in vivo confocal microscopy (IVCM) and multimodal corneal esthesiometry for structural and functional phenotyping and review emerging nerve-directed interventions. Integrating morphology, sensory function, and neuroimmune biology may improve the mechanistic classification of DED and support more precise treatment of patients with symptom-sign discordance.

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Cite

BibTeXRIS
BibTeX
@article{liu2026pathological,
  title = {{Pathological remodeling and functional evolution of the corneal nervous system in ocular surface dyshomeostasis.}},
  author = {Jiayang Liu and Hanwen Lu and Xiyao Liu},
  journal = {Frontiers in aging neuroscience},
  year = {2026},
  month = oct,
  doi = {10.3389/fnagi.2026.1946017},
  url = {https://europepmc.org/article/MED/42953486},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Pathological remodeling and functional evolution of the corneal nervous system in ocular surface dyshomeostasis.
AU  - Jiayang Liu
AU  - Hanwen Lu
AU  - Xiyao Liu
PY  - 2026
DA  - 2026/10/14
JO  - Frontiers in aging neuroscience
DO  - 10.3389/fnagi.2026.1946017
UR  - https://europepmc.org/article/MED/42953486
AB  - The corneal nerve plexus is essential to ocular surface homeostasis through sensory detection, trophic support, epithelial repair, blinking, and lacrimal reflexes. In dry eye disease (DED), chronic hyperosmolar, inflammatory, mechanical, and age-related stressors alter nerve morphology and function, contributing to reduced nerve density, aberrant regeneration, microneuroma formation, sensory loss, and peripheral or central sensitization. This review summarizes the ultrastructure of corneal innervation and the molecular basis of corneal sensory transduction, with emphasis on TRPM8, TRPV1, TRPA1, Piezo2, and acid-sensing ion channels. It then examines bidirectional neuroimmune signaling involving dendritic cells, cytokines, neuropeptides, and diminished neurotrophic support. We further discuss the relationship between age-related corneal hypoesthesia, local small-fiber degeneration, and systemic neurodegenerative disorders, while noting the limited disease specificity of currently proposed corneal biomarkers. Finally, we evaluate in vivo confocal microscopy (IVCM) and multimodal corneal esthesiometry for structural and functional phenotyping and review emerging nerve-directed interventions. Integrating morphology, sensory function, and neuroimmune biology may improve the mechanistic classification of DED and support more precise treatment of patients with symptom-sign discordance.
SN  - 1663-4365
ER  -