Suppression of MERTK inhibits proliferation and migration of pterygium fibroblasts.

About 10.2 % of people worldwide suffer from pterygium, a proliferative disorder marked by a wing-shaped growth that stretches from corneoscleral limbus to central area. MER proto-oncogene tyrosine kinase (MERTK) has been linked in recent research to the promotion of organ fibrosis and tumor growth. To look into its underlying function and mechanisms, we employed RNA-sequencing methods, MERTK inhibitors, and a series of tests. Primary human pterygium fibroblasts (HPFs) and pterygium tissues both exhibited high expression of MERTK. HPFs' migratory and proliferative capabilities were decreased by MERTK inhibition, which also encouraged an increase in apoptosis. Cell cycle arrest was mechanistically caused by MERTK inhibition. Additionally, further research revealed that this was linked to the downregulation of the ERK/p38 MAPK and PI3K/AKT signaling pathways In addition, MERTK expression was positively correlated with clinical grading, which indicates the degree of pterygium fibrosis. Collectively, targeting MERTK presents a potential therapeutic strategy to limit the proliferation, migration, and fibrosis associated with pterygium. This research may pave a promising way for more effective therapeutic approaches at controlling disease progression.