Dysregulated autophagy and suppressed apoptosis drive pterygium progression, elevating Beclin-1, ATG5, LC3, p62, Bcl-2.
Background
Pterygium is a common ocular surface disease characterized by a benign, fibrovascular growth that can encroach upon the cornea, leading to vision impairment. Current treatment primarily involves surgical excision, which carries risks of recurrence and complications. Understanding the underlying cellular mechanisms, particularly apoptosis (programmed cell death) and autophagy (cellular recycling), is crucial for developing non-surgical therapies. Dysregulation of these pathways is implicated in various proliferative disorders, suggesting they may play a key role in the persistent growth and progression of pterygium tissue.
Study Design
This prospective, observational, controlled study investigated apoptosis and autophagy in primary pterygium. Researchers compared excised pterygium tissues (study group) with normal conjunctival tissues obtained from autografts (control group). Immunohistochemical staining was employed to quantify the expression of autophagy-related proteins: Beclin-1, LC3A/B, ATG5, and p62, alongside apoptosis-related proteins: Bcl-2 and Caspase-8. Quantitative immunohistochemical evaluation utilized H-score analysis with Image Tool Software to assess protein expression levels.
Results
The study group demonstrated significantly elevated expression of several key proteins compared to controls. Beclin-1 expression was 97.65 ± 2.54 in pterygium vs. 25.53 ± 0.4 in normal tissue (p < 0.001). Similarly, LC3A/B increased from 61.73 ± 5.08 to 97.88 ± 5.35 (p < 0.001), and ATG5 from 35.35 ± 0.3 to 100.73 ± 1.06 (p < 0.001). Expression of p62 also rose from 59.54 ± 2.29 to 84.18 ± 3.59 (p < 0.001).
Key Findings
- Pterygium tissues showed significantly increased Beclin-1 expression (97.65 ± 2.54 vs. 25.53 ± 0.4, p < 0.001).
- LC3A/B expression was significantly higher in pterygium (97.88 ± 5.35 vs. 61.73 ± 5.08, p < 0.001).
- ATG5 expression was markedly elevated in pterygium (100.73 ± 1.06 vs. 35.35 ± 0.3, p < 0.001).
- Pterygium tissues exhibited increased p62 expression (84.18 ± 3.59 vs. 59.54 ± 2.29, p < 0.001).
- Bcl-2 expression was significantly higher in pterygium (107.36 ± 1.60 vs. 53.56 ± 1.38, p < 0.001).
Why It Matters
This research provides critical insights into the cellular pathology of pterygium, identifying specific biomarkers that could serve as targets for novel pharmacological interventions. Modulating autophagy and apoptosis pathways offers a promising non-surgical approach to manage pterygium progression. By targeting proteins like Beclin-1, ATG5, LC3, p62, or Bcl-2, it may be possible to inhibit the abnormal fibrovascular growth and reduce the need for surgical excision. This could lead to the development of topical or systemic treatments that prevent recurrence or even reverse early-stage pterygium, significantly improving patient outcomes and quality of life by offering a less invasive alternative.
pterygium
autophagy
apoptosis
ocular-disease
biomarker
pathogenesis