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Complement C5a Promotes Epithelial-Mesenchymal Transition in Pterygium via C5aR Activation
Jiaxin Han1,2, Qianwen Gong1,2, 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.
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.
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