ArticleJournal of radiation research2026
BMSCs alleviate inflammation and inhibit apoptosis in radiation pneumonitis treatment by modulating the NF-κB/NLRP3 signaling pathway.
Article in Journal of radiation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Radiation pneumonitis (RP) is a severe consequence of thoracic radiation, and its pathophysiology is tightly linked to NLRP3 inflammasome-mediated hyperinflammatory reactions. The nuclear factor κB (NF-κB) signaling system, which regulates NLRP3, could be a potential therapeutic target. This study explores how bone marrow-derived mesenchymal stem cells (BMSCs) can treat RP via modifying the NF-κB/NLRP3 signaling pathway. BMSCs treatment significantly reduced inflammatory infiltration in rat lung tissue and decreased inflammatory cytokine release. Mechanistically, by inhibiting the NF-κB/NLRP3 signaling axis, BMSCs consequently reduce the secretion of key pro-inflammatory mediators, including IL-1β, IL-18, and TNF-α. Additionally, BMSCs suppressed apoptosis by downregulating inflammasome formation, achieving therapeutic effects against RP. BMSCs block NF-κB/NLRP3 signaling, reducing inflammasome production. They treat RP by inhibiting inflammasomes and suppressing apoptosis. This strategy is a novel therapy option for RP management and clinical prevention.
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