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Thymidine induces macrophage M1 polarization in radiation-induced-lung-injury by ATF3/p38 pathway
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DOI:10.1016/j.cellimm.2026.105063.png)
Abstract
En 中文
• Radiation-induced lung injury (RILI) progression is mechanistically linked to macrophage polarization via epithelial metabolic remodeling rather than direct radiation damage. • Radiation-elevated thymidine drives M1 polarization, whose cytokine storms exacerbate alveolar epithelial injury. • Thymidine orchestrates M1 polarization through transcriptional repression of ATF3-coupled p38 MAPK signaling. • Blockade of Thymidine Uptake or ATF3 Signaling Attenuates Radiation-Induced Lung Injury in Murine Models.
Keywords:
Thymidine
Macrophage M1 polarization
Radiation-induced lung injury
ATF3
p38 MAPK pathway
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