Crosstalk between TRPV1 and immune regulation in Fuchs endothelial corneal dystrophy

Yuchen Cai1, Jin Chen1, Hao Sun1

  • 1Department of Ophthalmology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China.

Insights

Fuchs endothelial corneal dystrophy (FECD) involves Transient Receptor Potential Vanilloid 1 (TRPV1) and immune cells. This study identifies TRPV1-related genes and pathways, suggesting a new therapeutic target for FECD.

Area of Science:

  • Ophthalmology
  • Immunology
  • Molecular Biology

Background:

  • Fuchs endothelial corneal dystrophy (FECD) is a primary cause of corneal transplantation globally.
  • The role of Transient Receptor Potential Vanilloid subtype 1 (TRPV1) and immune regulation in FECD pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the involvement of TRPV1 and associated immune responses in FECD.
  • To identify key genes and pathways linking TRPV1 to FECD.

Main Methods:

  • Utilized an in vitro FECD model with H₂O₂ induction.
  • Analyzed gene expression microarray datasets (GSE142538, GSE112039, E-GEAD-399 & 564).
  • Performed functional analyses on TRPV1-related differentially expressed genes (DEGs) and in vitro validation.

Main Results:

  • TRPV1 was significantly upregulated in the in vitro FECD model.
  • A negative correlation was observed between TRPV1 expression and immune cells, particularly regulatory T cells (Tregs).
  • Identified four core TRPV1-related genes (MAPK14, GNB1, GNAQ, ARRB2) and implicated TRP-regulated calcium transport and inflammatory pathways.

Conclusions:

  • TRPV1 and immune regulation exhibit potential crosstalk in FECD pathogenesis.
  • The identified biomarkers and pathways offer a novel framework for FECD research and therapeutic development.