# Far Infrared Radiation Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice via Modulation of the p53/TGF-β Signaling Pathway

**Authors:** Jicheng Li, Jingxu Chang, Wenhan Chu, Yu Jiang, Shaodi Sun, Xiaodi Ding, Liying Zhang, Lihong Shi

PMC · DOI: 10.3390/ijms27062551 · International Journal of Molecular Sciences · 2026-03-10

## TL;DR

Far infrared radiation reduces lung fibrosis in mice by targeting a key signaling pathway, offering a non-invasive treatment for pulmonary fibrosis.

## Contribution

This study is the first to demonstrate FIR's anti-fibrotic effects and its mechanism via the p53/TGF-β pathway in a mouse model of pulmonary fibrosis.

## Key findings

- FIR therapy improved lung function and reduced fibrosis in bleomycin-treated mice.
- FIR inhibited fibroblast differentiation and epithelial-mesenchymal transition in fibrotic lungs.
- FIR's effects were mediated through modulation of the p53/TGF-β signaling pathway.

## Abstract

Currently, there is no curative medication for idiopathic pulmonary fibrosis (IPF), and therapeutic interventions for IPF are hindered by limited efficacy and severe adverse side effects. Far Infrared Radiation (FIR), an invisible form of electromagnetic energy, has garnered increasing attention for its multiple biological effects. However, its therapeutic benefits and the underlying mechanisms of IPF have not been investigated. In the present study, we established a mouse model of bleomycin-induced pulmonary fibrosis (BIPF) to assess the efficacy of FIR in attenuating BIPF. The results showed that FIR therapy significantly improved the general condition of the mice and protected pulmonary function by ameliorating lung fibrosis, collagen deposition and excessive inflammation. Moreover, FIR could alleviate fibroblast-to-myofibroblast differentiation (FMD), the epithelial–mesenchymal transition (EMT) and angiogenesis in BIPF mice. These beneficial effects were notable both in the pro-fibrotic inflammatory stage and the following fibrotic stage. Mechanistically, FIR exerted anti-inflammatory and anti-fibrotic effects through modulating the p53/TGF-β signaling pathway. Overall, this study elucidates the anti-fibrotic activity and the potential molecular mechanisms of FIR in treating BIPF, providing a therapeutic strategy of convenient, non-invasive physical therapy for alleviating IPF. Of greater significance, the findings of this study display the promising future applications of FIR in managing the physiopathology of various chronic diseases.

## Linked entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157], TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040]
- **Chemicals:** bleomycin (PubChem CID 5360373)
- **Diseases:** idiopathic pulmonary fibrosis (MONDO:0800029), pulmonary fibrosis (MONDO:0002771)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Trp53-ps (transformation related protein 53, pseudogene) [NCBI Gene 22060], Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}
- **Diseases:** BIPF (MESH:D011658), inflammation (MESH:D007249), lung fibrosis (MESH:D005355), IPF (MESH:D054990)
- **Chemicals:** Bleomycin (MESH:D001761)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13026882/full.md

## References

63 references — full list in the complete paper: https://tomesphere.com/paper/PMC13026882/full.md

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Source: https://tomesphere.com/paper/PMC13026882