Condition Focus: Fibrotic Tissue Remodeling — Whole Transcriptome Analysis
Rather than testing a handful of pre-selected genes, this study from Jagdeo and colleagues at Stanford took an unbiased approach: whole transcriptome analysis using RNA sequencing to capture every gene expression change in human dermal fibroblasts following red light PBM. Published in Nature’s Scientific Reports, this is among the most comprehensive molecular analyses of PBM’s effects on fibroblast biology.
Two genes stood out with the most significant changes. MMP1 (matrix metalloproteinase-1) was upregulated — this is the primary enzyme responsible for breaking down type I collagen, the structural protein of fibrotic scar tissue. In the context of fibrosis, MMP1 upregulation is therapeutically desirable because it promotes the remodeling and removal of excessive collagen deposits.
PRSS35 (a serine protease) showed a remarkable 30-fold upregulation. While less well-characterized than MMP1, PRSS35 is emerging as a significant anti-fibrotic factor. Its dramatic upregulation by PBM suggests it may be one of the key effector genes through which light therapy counteracts pathological fibrosis.
The study also observed modulation of SMAD3, SMAD4, and SMAD7 — components of the TGF-β signalling pathway that drives fibroblast activation and collagen production. This connects the transcriptomic findings to the same pathway identified in the keloid and fibrosis reviews in this library.
For chronic tophaceous gout, MMP1-mediated collagen remodeling could potentially help break down the fibrotic shell surrounding tophi, facilitating their resolution. This is speculative but mechanistically grounded — the enzyme and the target are correctly matched.
G.O.A.T. for Gout Alignment:
Red light PBM — the 660 nm component of the G.O.A.T. — activates the specific anti-fibrotic genes (MMP1, PRSS35) and pathway modulators (SMADs) relevant to tophaceous tissue remodeling. This transcriptomic evidence provides molecular-level support for the G.O.A.T.’s potential role in chronic gout management.
Link to original research here
Editor’s note: The MMP1 upregulation here provides the molecular mechanism for the anti-fibrotic effects reviewed in PBM in Keloid Management 2025 and PBM and Fibrosis Prevention 2025. The SMAD pathway modulation connects to the TGF-β cascade. The dual anti-inflammatory + anti-fibrotic effect at 660 nm is demonstrated in vivo by Brochetti et al 2017. The MMP-13 suppression that protects cartilage (rather than breaks down fibrosis) is a different MMP with a different tissue target — see Nambi 2021.
Related Articles
- PBM in Keloid Management: Anti-Fibrotic Mechanisms – 2025
- PBM as Prevention/Treatment for Fibrosis – 2025
- PBM Improves Inflammatory and Fibrotic Parameters – Brochetti et al 2017
- LLLT Effects on Inflammatory Biomarkers in OA: Meta-Analysis – Nambi 2021
- PBM in Promoting Cartilage Regeneration – 2025
Key Takeaways
- Whole transcriptome analysis — unbiased, genome-wide gene expression profiling
- MMP1 upregulated — the primary enzyme for breaking down fibrotic collagen deposits
- PRSS35 upregulated 30-fold — emerging anti-fibrotic factor, novel PBM target
- SMAD3/4/7 modulation connects to TGF-β fibrosis pathway
Study Overview
| Study Type: | In vitro (whole transcriptome, RNA-seq) |
| Wavelength(s): | Red light (specific wavelength not reported) |
| Treatment Protocol: | 320, 640 J/cm²; human dermal fibroblasts |
| Sample Size: | Human fibroblast cultures with RNA-seq |
| Primary Outcome: | MMP1↑ (collagen remodeling); PRSS35↑ 30x (anti-fibrotic); SMAD modulation |
Full Citation
Jagdeo J, et al. (2021). Transcriptomic analysis of human dermal fibroblasts following red light phototherapy. Scientific Reports, 11, 7315. View Publication
