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1
Traumatic lung injury (TLI) can lead to acute respiratory distress syndrome (ARDS), which has a high mortality rate and limited targeted therapies.
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2
Single-cell RNA sequencing revealed that ISG15+STAT1+ monocytes expand post-trauma and drive an inflammatory response through M1-like polarization.
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3
PIM1 was identified as a core pathogenic gene co-upregulated in both peripheral blood and lung tissue, confirmed as a causal risk factor for ARDS.
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4
The JAK2/STAT3/PIM1 signaling pathway is activated during the acute trauma phase, contributing to the inflammatory response in TLI.
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5
Fedratinib, a JAK2 inhibitor, was shown to inhibit M1 polarization and inflammatory gene expression, suggesting its potential as a therapeutic candidate for TLI.