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Induction of Ocular Surface Inflammation and Collection of Involved Tissues

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Published on: August 4, 2022

Recent progress in N6-methyladenosine modification in ocular surface diseases.

Wei Wang¹, Jun Zou¹

¹Department of Ophthalmology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200072, China.

International Journal of Ophthalmology

|April 20, 2023

Summary

N6-methyladenosine (m6A) modification plays a crucial role in ocular surface diseases (OSDs). Understanding m6A regulation offers new therapeutic insights for conditions like fungal keratitis and Graves' ophthalmopathy.

Keywords:

N6-methyladenosine epigenetics m6A modification ocular surface diseases

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A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues

Published on: December 5, 2016

Area of Science:

Epigenetics
Ophthalmology
Molecular Biology

Background:

N6-methyladenosine (m6A) is a key reversible epigenetic modification.
Dysregulation of m6A is implicated in various diseases.
m6A modification is increasingly recognized for its role in ocular surface diseases (OSDs).

Purpose of the Study:

To review the role of m6A modification in the pathogenesis of OSDs.
To summarize current research progress on m6A in various OSDs.
To explore potential therapeutic applications of targeting m6A in OSDs.

Main Methods:

Literature review of studies investigating m6A modification in OSDs.
Analysis of research on m6A 'writers', 'erasers', and 'readers' in ocular contexts.
Synthesis of findings related to specific OSDs including keratitis, pterygium, and Graves' ophthalmopathy.

Main Results:

m6A modification is closely linked to the development and progression of diverse OSDs.
Specific OSDs reviewed include fungal keratitis, herpes simplex keratitis, immune-related keratoconjunctival diseases, pterygium, ocular chemical burns, and Graves' ophthalmopathy.
Aberrant m6A regulation contributes to pathological cellular behaviors in OSDs.

Conclusions:

m6A modification is a significant factor in the pathophysiology of OSDs.
Further research into m6A mechanisms in OSDs may yield novel diagnostic and therapeutic strategies.
Targeting m6A pathways presents a promising avenue for future OSD treatments.