A novel lncRNA enhances autophagy to suppress extracellular matrix via modulating TP53INP1 in human trabecular meshwork cells under oxidative stress.

ABSTRACT: Primary open-angle glaucoma (POAG) can result in irreversible blindness. As an important etiological factor, oxidative stress can elicit extraordinary increase of extracellular matrix (ECM) in trabecular meshwork-schlemm canal, to increase aqueous humor outflow resistance and elevate intraocular pressure. Although autophagy plays an important role in clearing ECM, the functions of long non-coding RNAs (lncRNAs) in autophagy induced by oxidative stress in human trabecular meshwork cells (HTMCs) remain unclear. In our study, oxidative stress induced the expression of ECM and autophagy in TMCs after H₂O₂ treatment. Meanwhile, a novel lncRNA ENST00000523905 and tumor protein 53-induced nuclear protein 1 (TP53INP1) were elevated in TMCs treated with H₂O₂

SUBMITTER: Tie J 

PROVIDER: S-EPMC11814328 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature