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Updated: Feb 19, 2026

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
Published on: September 20, 2024
The JAK1-STAT1 signaling pathway triggers inflammation responses in chronic obstructive sleep apnea rat model
1Department of Pulmonary and Critical Care Medicine, Huili People's Hospital, Liangshan Yi Autonomous Prefecture, Huili, Sichuan, China.
Background:
Chronic obstructive sleep apnea (OSA) drives systemic inflammation; the role of the JAK1-STAT1 pathway is unclear.
Objective:
To elucidate JAK1-STAT1 involvement in OSA-related inflammation using a chronic intermittent hypoxia (CIH) model.
Methods:
Sprague-Dawley rats underwent 8-week CIH (FiO₂ cycling 5-21%, 8h/day) or normoxia (Sham). Serum cytokines (ELISA) and lung p-JAK1/p-STAT1 (Western blot/IHC) were analyzed. A CIH subset received JAK1 inhibitor filgotinib. Airway resistance was assessed via forced oscillation.
Results:
CIH elevated serum IL-6/TNF-α versus Sham (p < 0.05) and increased lung p-JAK1/p-STAT1. Filgotinib reduced cytokines, suppressed p-JAK1/p-STAT1, attenuated leukocyte infiltration/collagen deposition, and improved airway resistance. Lung p-STAT1 strongly correlated with serum IL-6 (r = 0.86) and TNF-α (r = 0.82) (both p < 0.001).
Conclusion:
JAK1-STAT1 signaling critically mediates CIH-induced inflammation. JAK1 inhibition attenuates inflammatory responses, demonstrating therapeutic potential for OSA comorbidities.
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