# Photobiomodulation Therapy: The Dawn of Myopia Control

**Authors:** Kate Gettinger, Yinuo Huang, Kazuo Tsubota, Kazuno Negishi, Toshihide Kurihara

PMC · DOI: 10.3390/cells15060526 · 2026-03-16

## TL;DR

This review explores how light exposure, especially red, blue, and violet light, may help control myopia by influencing eye development through complex biological mechanisms.

## Contribution

The paper reviews recent findings on photobiomodulation as a potential strategy for myopia prevention, emphasizing the role of specific light wavelengths.

## Key findings

- Red, blue, and violet light exposure may help control axial growth and refractive changes linked to myopia.
- Nonvisual opsins and spectrum-specific influences play a role in the complex pathways of light's effect on myopia development.
- Photobiomodulation shows promise as an intervention, but the underlying mechanisms remain incompletely understood.

## Abstract

What are the main findings?
Light exposure potentially influences myopia development through a variety of proposed mechanisms, although a full understanding of the mechanisms is still lacking.Recent research into the role of nonvisual opsins and spectrum-specific influences on myopia development has highlighted the complexity of these potential pathways.

Light exposure potentially influences myopia development through a variety of proposed mechanisms, although a full understanding of the mechanisms is still lacking.

Recent research into the role of nonvisual opsins and spectrum-specific influences on myopia development has highlighted the complexity of these potential pathways.

What are the implications of the main findings?
Future myopia prevention strategies may utilize promising findings featuring both red, blue, and violet light exposure as a means to control axial growth and refractive changes.While there is still much to be explored, recent findings have suggested several potential mechanisms through which light influences myopia development.

Future myopia prevention strategies may utilize promising findings featuring both red, blue, and violet light exposure as a means to control axial growth and refractive changes.

While there is still much to be explored, recent findings have suggested several potential mechanisms through which light influences myopia development.

As the prevalence of myopia, or near-sightedness, continues to rise globally, it becomes imperative to determine the mechanisms driving myopia so that appropriate interventions to mitigate it can be developed. Light appears to be critical for normal ocular development, and over the past several decades research has explored the connection between light exposure and myopia development. This review explores the growing field of photobiomodulation, or the use of light to modulate biological processes, to prevent myopia development. To complete this review, relevant texts published from January 1990 to December 2025 were retrieved from the PubMed database using a combination of search terms covering myopia and ocular development, light exposure conditions related to myopia, myopia development in relation to circadian and diurnal regulation, nonvisual opsins and myopia, and light-induced ocular damage. Through this review, we see that photobiomodulation offers a potential intervention to control myopia progression, but the mechanisms behind light’s influence on ocular development remain complex and incompletely understood. This review aims to summarize what is currently known to serve as a basis for future research and to delineate important findings.

## Linked entities

- **Diseases:** myopia (MONDO:0001384)

## Full-text entities

- **Genes:** OPN1MW (opsin 1, medium wave sensitive) [NCBI Gene 2652] {aka CBBM, CBD, COD5, GCP, GOP, OPN1MW1}, OPN5 (opsin 5) [NCBI Gene 221391] {aka GPR136, GRP136, PGR12, TMEM13}, Pdlim5 (PDZ and LIM domain 5) [NCBI Gene 56376] {aka 1110001A05Rik, Enh, Enh1, Enh2, Enh3, LIM}, Opn1sw (opsin 1 (cone pigments), short-wave-sensitive (color blindness, tritan)) [NCBI Gene 12057] {aka Bcp}, Vsx2 (visual system homeobox 2) [NCBI Gene 12677] {aka Chx10, Hox-10, Hox10, or}, Opn3 (opsin 3) [NCBI Gene 13603] {aka ERO, Ecpn}, Egr1 (early growth response 1) [NCBI Gene 13653] {aka A530045N19Rik, ETR103, Egr-1, Krox-1, Krox-24, Krox24}, NOS [NCBI Gene 100135576], Bmal1 (basic helix-loop-helix ARNT like 1) [NCBI Gene 11865] {aka Arnt3, Arntl, BMAL1b, MOP3, bHLHe5, bmal1b'}, OPN1SW (opsin 1, short wave sensitive) [NCBI Gene 611] {aka BCP, BOP, CBT}, OPN3 (opsin 3) [NCBI Gene 23596] {aka ECPN, PPP1R116}, EGR1 (early growth response 1) [NCBI Gene 1958] {aka AT225, G0S30, KROX-24, NGFI-A, TIS8, ZIF-268}, Opn5 (opsin 5) [NCBI Gene 353344] {aka Gpr136, Neuropsin, PGR12, TMEM13}, Opn4 (opsin 4 (melanopsin)) [NCBI Gene 30044] {aka 1110007J02Rik, Gm533}, Camp (cathelicidin antimicrobial peptide) [NCBI Gene 12796] {aka CAP18, CLP, Cnlp, Cramp, FALL39, MCLP}, OPN4 (opsin 4) [NCBI Gene 94233] {aka MOP}, Rho (rhodopsin) [NCBI Gene 212541] {aka Noerg1, Opn2, Ops, RP4}, OPN1LW (opsin 1, long wave sensitive) [NCBI Gene 5956] {aka CBBM, CBP, COD5, RCP, ROP}
- **Diseases:** RPE damage (MESH:D020263), reduced axial elongation (MESH:D001523), aphakia (MESH:D001035), periocular tumors (MESH:D019557), solar retinopathy (MESH:D000092130), chorioretinal atrophy (MESH:C566236), outer retinal defects (MESH:D012173), Form (MESH:C565541), dizziness (MESH:D004244), injury to (MESH:D014947), cataract (MESH:D002386), retinal detachment (MESH:D012163), myopic (MESH:D001251), pterygium (MESH:D011625), choroidal thinning (MESH:D013851), nuclear and posterior subcapsular cataracts (MESH:C565137), axial elongation (MESH:C537791), anxiety (MESH:D001007), LCA (MESH:C566125), Myopia (MESH:D009216), COVID-19 (MESH:D000086382), reduced vision (MESH:D015354), attention deficit hyperactivity disorder (MESH:D001289), scotoma (MESH:D012607), elongation (MESH:C538010), FDM (MESH:D012892), retinal UV damage (MESH:D012164), epithelial (MESH:D009375), aberration (MESH:D002869), ocular damage (MESH:D015817), blindness (MESH:D001766), ametropia (MESH:D012030), age-related macular degeneration (MESH:D008268), optic disc abnormalities (MESH:D009901), fibrosis (MESH:D005355), ocular diseases (MESH:D005128), binocular vision loss (MESH:D014786), sleep disruptions (MESH:D019958), LLRL (MESH:D009800), hyperopia (MESH:D006956), cutaneous melanoma (MESH:C562393)
- **Chemicals:** DTA (MESH:C042899), FDM (-), NO (MESH:D009569), cGMP (MESH:D006152), MPH (MESH:D008774), 3,4-Dihydroxyphenylacetic Acid (MESH:D015102), 8-OHdG (MESH:D000080242), Dopamine (MESH:D004298), L-DOPA (MESH:D007980), all-trans retinoic acid (MESH:D014212), Melatonin (MESH:D008550), reactive oxygen species (MESH:D017382)
- **Species:** Homo sapiens (human, species) [taxon 9606], Cavia porcellus (domestic guinea pig, species) [taxon 10141], Gallus gallus (bantam, species) [taxon 9031], Drosophila melanogaster (fruit fly, species) [taxon 7227], Macaca mulatta (rhesus macaque, species) [taxon 9544], Mus musculus (house mouse, species) [taxon 10090], Macaca fascicularis (crab eating macaque, species) [taxon 9541], Oryctolagus cuniculus (domestic rabbit, species) [taxon 9986]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13025185/full.md

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Source: https://tomesphere.com/paper/PMC13025185