mTORC1 regulates apoptosis and cell proliferation in pterygium via targeting autophagy and FGFR3

Area of Science:

• Ophthalmology
• Cell Biology
• Molecular Biology

Background:

• Pterygium is a prevalent ocular surface disease characterized by aberrant epithelial cell behavior.
• The role of Mechanistic Target of Rapamycin Complex 1 (mTORC1) in pterygium initiation, including its effects on apoptosis and proliferation, remains largely unknown.

Purpose of the Study:

• To investigate the activation status and functional role of mTOR signaling, particularly mTORC1, in pterygium development.
• To elucidate the mechanisms by which mTORC1 influences aberrant apoptosis and cell proliferation in pterygium.

Main Methods:

• Evaluation of mTOR signaling pathway activation in pterygium tissues.
• Analysis of apoptosis and cell proliferation markers in relation to mTORC1 activity.
• Investigation of mTORC1's regulatory effects on autophagy (Beclin 1, Bcl-2) and FGFR3/p73 signaling.

Main Results:

• mTOR signaling, specifically mTORC1, is significantly activated in pterygium.
• mTORC1 activation was associated with both inhibited apoptosis and increased cell proliferation.
• mTORC1 inhibits apoptosis by modulating Beclin 1-dependent autophagy via Bcl-2 targeting.
• mTORC1 promotes cell proliferation by negatively regulating FGFR3 through p73 inhibition.

Conclusions:

• mTORC1 signaling is highly active in pterygium, contributing to its pathogenesis.
• mTORC1 plays a critical role in regulating aberrant apoptosis and cell proliferation during pterygium progression.
• Targeting mTORC1 may offer a novel therapeutic strategy for treating pterygium.