Autophagy-related pathway dysregulation and apoptosis suppression in pterygium: Role of key biomarkers Beclin-1, ATG5, LC3, p62, and Bcl-2 in pathogenesis and potential nonsurgical targets.

ObjectivesTo investigate the roles of apoptosis and autophagy in the pathogenesis of primary pterygium and to evaluate potential biomarkers that could lead to nonsurgical therapeutic approaches.MethodsIn this prospective, observational, controlled study, patients diagnosed with primary pterygium were included. Excised pterygium tissues (study group) were compared with normal conjunctival tissues obtained from autografts (control group). Immunohistochemical staining was used to assess the expression of autophagy-related proteins (Beclin-1, LC3A/B, ATG5, and p62) and apoptosis-related proteins (Bcl-2 and Caspase-8). Quantitative immunohistochemical evaluation was performed using H-score analysis with Image Tool Software.ResultsThe study group exhibited significant increases in the expression of Beclin-1 (97.65 ± 2.54 vs. 25.53 ± 0.4), LC3A/B (97.88 ± 5.35 vs. 61.73 ± 5.08), ATG5 (100.73 ± 1.06 vs. 35.35 ± 0.3), p62 (84.18 ± 3.59 vs. 59.54 ± 2.29), and Bcl-2 (107.36 ± 1.60 vs. 53.56 ± 1.38) compared with the control group (p < 0.001 for all). Although Caspase-8 expression was also increased (65 ± 1.53 vs. 49 ± 0.2), the difference was not statistically significant (p = 0.270). These findings suggest altered regulation of autophagy-related pathways accompanied by suppression of apoptotic mechanisms, which may contribute to the persistence, fibrovascular proliferation, and progression of pterygium tissue.ConclusionThe progression of pterygium appears to be associated with dysregulation of autophagy-related pathways and inhibition of apoptotic mechanisms. These findings suggest that modulation of these cellular mechanisms may provide novel pharmacological therapeutic options, potentially reducing the need for surgical intervention.