The Role of circFAM53B in Regulating Choroidal Vascular Function in Pathological Myopia

Area of Science:

• Ophthalmology
• Molecular Biology
• Genetics

Background:

• Myopia is a global epidemic with pathological forms causing irreversible vision loss.
• Choroidal dysfunction is a key factor in pathological myopia progression.
• Understanding the molecular mechanisms of choroidal dysfunction is crucial for developing effective treatments.

Purpose of the Study:

• To investigate the role of circular RNA circFAM53B in choroidal dysfunction in pathological myopia.
• To explore the molecular mechanisms underlying circFAM53B's involvement in myopia progression.

Main Methods:

• Established in vitro and in vivo models of hypoxic and oxidative injury to mimic choroidal dysfunction.
• Utilized RNA sequencing and bioinformatics to analyze circular RNA expression.
• Performed functional assays and mechanistic studies to elucidate circFAM53B's function and interactions.

Main Results:

• circFAM53B was consistently upregulated in injured choroidal cells and in a guinea pig myopia model.
• Knockdown of circFAM53B improved choroidal endothelial cell viability, migration, and tubulogenesis while reducing apoptosis.
• circFAM53B acts as a sponge for miR-1248, upregulating its target THBS1.

Conclusions:

• The circFAM53B/miR-1248/THBS1 pathway is implicated in choroidal dysfunction in pathological myopia.
• This pathway offers potential therapeutic targets for myopia-related complications.
• Findings expand the understanding of molecular mechanisms driving myopia development.