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Complement C5a Promotes Epithelial-Mesenchymal Transition in Pterygium via C5aR Activation.

Jiaxin Han^1,2, Qianwen Gong^1,2, He Wang³

¹National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, People's Republic of China.

Investigative Ophthalmology & Visual Science

|June 10, 2026

Summary

Complement component 5a (C5a) signaling drives pterygium development by promoting epithelial-mesenchymal transition in conjunctival cells. Targeting C5a receptor (C5aR) may offer a novel therapeutic strategy for pterygium.

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Published on: June 15, 2019

Area of Science:

Ophthalmology
Immunology
Proteomics

Background:

Pterygium is a common ocular surface disease characterized by abnormal fibrovascular growth.
The underlying molecular mechanisms of pterygium pathogenesis remain incompletely understood.

Purpose of the Study:

To identify regulatory proteins involved in pterygium pathogenesis.
To investigate the biological roles of these candidate proteins in disease development.

Main Methods:

Proteomic analysis (label-free/4D label-free) of pterygium and conjunctival tissues.
Functional validation using primary conjunctival epithelial cells (PCECs) stimulated with C5a and C5a receptor antagonist PMX53.
Assays included epithelial-mesenchymal transition (EMT) markers, cell migration, apoptosis, and VEGFA expression.

Main Results:

Complement component 5 (C5) was upregulated in pterygium tissues and correlated positively with vessel density.
C5a promoted EMT-like changes in PCECs, including decreased E-cadherin and increased vimentin and fibronectin.
C5a enhanced cell migration, reduced apoptosis, and increased VEGFA expression, effects attenuated by PMX53.

Conclusions:

C5a/C5aR signaling contributes to pterygium pathogenesis by inducing EMT in conjunctival epithelial cells.
C5a receptor (C5aR) represents a potential therapeutic target for pterygium.