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Rapamycin protects glucocorticoid-induced glaucoma model mice against trabecular meshwork fibrosis by suppressing

Yuning Song1, Feifei Wang2, Hongdou Luo1

  • 1Affiliated Eye Hospital of Nanchang University, Jiangxi Medical College, Nanchang University, Jiangxi Research Institute of Ophthalmology & Visual Science, Jiangxi Provincial Key Laboratory for Ophthalmology, Jiangxi Clinical Research Center for Ophthalmic Disease, Nanchang, China.

European Journal of Pharmacology
|January 13, 2025
PubMed

Insights

Rapamycin (Rapa) protects against glucocorticoid-induced glaucoma (GIG) by reducing intraocular pressure (IOP) and trabecular meshwork (TM) damage. It inhibits fibrosis and cytoskeletal changes, offering a new therapeutic avenue for GIG.

Area of Science:

  • Ophthalmology
  • Pharmacology
  • Cell Biology

Background:

  • Glucocorticoids (GCs) can cause pathological intraocular pressure (IOP) elevation, leading to vision loss.
  • Rapamycin (Rapa) is known for neuroprotective effects via inhibiting retinal glial cell activation and neuroinflammation.
  • The effect of Rapa on the trabecular meshwork (TM) in glaucoma remains under-investigated.

Purpose of the Study:

  • To investigate the protective effects and underlying mechanisms of Rapamycin (Rapa) in a glucocorticoid-induced glaucoma (GIG) model.
  • To determine if Rapa can mitigate IOP elevation, TM fibrosis, and retinal glial cell (RGC) damage caused by glucocorticoids.

Main Methods:

  • Established a glucocorticoid-induced glaucoma (GIG) model.
  • Administered Rapa to assess its impact on IOP, TM fibrosis, and RGC damage.
  • Utilized cultured human trabecular meshwork cells (HTMCs) treated with dexamethasone (Dex) and Rapa to analyze cellular changes and pathway activation.

Main Results:

  • Rapa significantly inhibited dexamethasone acetate (Dex-Ac)-induced IOP increase in the GIG model.
  • Rapa treatment improved TM fibrosis and reduced RGC damage.
  • In vitro, Rapa suppressed dexamethasone (Dex)-induced HTMC fibrosis and cytoskeletal alterations, potentially via mTORC1 and/or mTORC2 pathway inhibition.

Conclusions:

  • Rapa demonstrates significant protective effects against glucocorticoid-induced glaucoma (GIG).
  • The mechanism involves inhibiting TM fibrosis and cytoskeletal changes, possibly through modulation of mTORC1/mTORC2 pathways.
  • This study provides a novel theoretical basis for Rapa as a potential treatment for GIG.
Keywords:
DexamethasoneFibrosisGlaucomaRapamycinTrabecular meshworkmTOR

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