Condition Focus: Fibrosis Prevention — Myofibroblast Transition Inhibition
Fibrosis — the excessive deposition of collagen and extracellular matrix that replaces functional tissue with scar — is driven by the transition of normal fibroblasts into myofibroblasts. These activated cells produce collagen at dramatically increased rates and are resistant to the normal apoptosis signals that would limit their activity. This systematic review in PeerJ examines PBM’s ability to prevent and reverse this pathological transition.
The review covers multiple fibrosis models including radiation-induced fibrosis, chemical fibrosis, cryolesion, Duchenne muscular dystrophy fibrosis, and oral submucous fibrosis. Across these diverse models, PBM consistently inhibited the fibroblast-to-myofibroblast transition, reduced ECM and collagen production, promoted anti-inflammatory effects, enhanced angiogenesis (new blood vessel formation supporting tissue repair), and reduced ROS.
The 660 nm wavelength was the most commonly used across included studies, with energy densities typically in the 1–10 J/cm² range. The review notes that PBM’s anti-fibrotic effects are most pronounced when treatment is initiated early — before fibrosis is fully established — suggesting a preventive application in conditions where fibrosis risk is known.
For chronic gout, the preventive angle is particularly relevant. Patients with frequent flares are at known risk for tophaceous fibrosis. A maintenance PBM protocol could potentially slow or prevent the fibrotic remodeling that accompanies chronic crystal deposition — not just treating established tophi but preventing their development.
G.O.A.T. for Gout Alignment:
The G.O.A.T.’s 660 nm wavelength matches the most commonly effective wavelength for anti-fibrotic effects in this review. The preventive application — using maintenance PBM to prevent fibrotic remodeling — aligns with the G.O.A.T.’s 3x/week maintenance protocol for chronic gout management.
Link to original research here
Editor’s note: The myofibroblast transition inhibited here is the same cellular event that produces the fibrotic shell around tophi. The transcriptomic evidence for anti-fibrotic gene activation is in Jagdeo et al 2021. The TGF-β1/Smad pathway context is provided by PBM in Keloid Management 2025. The 660 nm dual anti-inflammatory + anti-fibrotic effect is demonstrated in Brochetti et al 2017.
Related Articles
- Transcriptome Analysis: Red Light Activates Anti-Fibrotic Genes – Jagdeo et al 2021
- PBM in Keloid Management: Anti-Fibrotic Mechanisms – 2025
- PBM Improves Inflammatory and Fibrotic Parameters – Brochetti et al 2017
- PBM, Cells of Connective Tissue and Repair – Houreld et al 2022
- PBM in Promoting Cartilage Regeneration – 2025
Key Takeaways
- PBM inhibits fibroblast-to-myofibroblast transition — the cellular driver of pathological fibrosis
- ECM and collagen overproduction reduced across multiple fibrosis models
- 660 nm most commonly effective wavelength for anti-fibrotic effects
- Early/preventive treatment more effective — supports maintenance PBM for at-risk gout patients
Study Overview
| Study Type: | Systematic review |
| Wavelength(s): | 660 nm (most common); 1–10 J/cm² |
| Treatment Protocol: | Varies; preventive and treatment applications |
| Sample Size: | Review of multiple fibrosis models |
| Primary Outcome: | Fibroblast→myofibroblast inhibition; ECM/collagen↓; ROS↓; angiogenesis↑ |
Full Citation
Potential role of photobiomodulation as prevention and treatment for fibrosis. (2025). PeerJ, 13, e19457. View Publication
