Why the study?
Viral-fibrotic sequelae are difficult to manage due to limited biomarkers, therapies, and unclear underlying mechanisms, including correlations between post-influenza gene expression, protein interactions, and pathophysiology.
Population
Time-course influenza infection model in mice
Comparison
Inhibition of PDIA3 evaluated against influenza-induced lung fibrosis and pathophysiology
Design
Preclinical animal study with transcriptomic network analysis
Key result
Inhibition of PDIA3 in influenza-infected mice downregulated ~50 transcripts associated with UPR and lung pathophysiological responses, decreasing influenza-induced pathophysiology and lung fibrosis.
Authors
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May identify targets for post-viral fibrosis; leaves open translation to human biomarkers or therapies.
Inhibition of PDIA3 reduces influenza-induced lung pathophysiology and fibrosis in mice by modulating UPR-related gene expression.
Kumar et al. (2026) studied Influenza infection and lung fibrosis. PDIA3 inhibition was evaluated on Correlation of gene modules with oxygen saturation (%SpO2) and collagen deposition. Inhibition of PDIA3 in influenza-infected mice downregulated ~50 transcripts associated with UPR and lung pathophysiological responses, decreasing influenza-induced pathophysiology and lung fibrosis.