ArticleInternational journal of biological sciences2024
Serum amyloid A contributes to radiation-induced lung injury by activating macrophages through FPR2/Rac1/NF-κB pathway.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- SAA/FPR2 Signaling Between Pericentral Hepatocytes and Macrophages Exacerbates Zonated Liver Transplant Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tumour-derived SAA1 reprogrammes macrophages to promote CXCL1-mediated metastasis in Ovarian Cancer.Clinical and translational medicine · 2026Article
- Serum amyloid A1 promote progression of breast cancer and is associated with epithelial-mesenchymal transition.Translational cancer research · 2026Article
- Multi-omics analysis unveils inflammatory and metabolic alterations between the synovium and cartilage in patients with knee osteoarthritis.Frontiers in molecular biosciences · 2026Article
- The role of macrophages in radiation-induced lung injury: from pathological mechanisms to therapeutic targets.Frontiers in immunology · 2026Review
- Serum amyloid A: multifaceted roles in inflammation and cellular interactions.Immunologic research · 2025Review
- Multi-omics data reveal that SAA1 + fibroblasts exacerbate periodontitis by regulating macrophage inflammation and chemotaxis.Journal of translational medicine · 2025Article
- Radiation-induced lung injury: from mechanism to prognosis and drug therapy.Radiation oncology (London, England) · 2025Review
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Authors and funding
8 authors.
Funding
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Abstract
Patients who receive thoracic radiotherapy may suffer from radiation-induced lung injury, but the treatment options are limited as the underlying mechanisms are unclear. Using a mouse model of right thorax irradiation with fractionated doses of X-rays for three consecutive days (8 Gy/per day), this study found that the thoracic irradiation (Th-IR) induced tissue injury with aberrant infiltration of macrophages, and it significantly increased the secretion of TNF-α, IL-1β, IL-6, TGF-β1 and serum amyloid A (SAA) in mice. Interestingly, SAA could activate macrophages and then induce epithelial-mesenchymal transition (EMT) of lung epithelial cells and fibrosis progression in lung tissue. Mechanistically, SAA enhanced the transient binding of FPR2 to Rac1 protein and further activated NF-κB signaling pathway in macrophages. Inhibition of FPR2 significantly reduced pulmonary fibrosis induced by SAA administration in mice. In addition, cimetidine could reduce the level of SAA release after irradiation and attenuate the lung injury induced by SAA or Th-IR. In conclusion, our results demonstrated that SAA activated macrophages via FPR2/Rac1/NF-κB pathway and might contribute to the Th-IR induced lung injury, which may provide a new strategy to attenuate radiation-induced adverse effects during radiotherapy.
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