2. Academic Validation
  3. The JAK1-STAT1 signaling pathway triggers inflammation responses in chronic obstructive sleep apnea rat model

The JAK1-STAT1 signaling pathway triggers inflammation responses in chronic obstructive sleep apnea rat model

  • PLoS One. 2026 Feb 17;21(2):e0343053. doi: 10.1371/journal.pone.0343053.
Lin Yang 1,  Jie He 2
Affiliations

Affiliations

  • 1 Department of Pulmonary and Critical Care Medicine, Huili People's Hospital, Liangshan Yi Autonomous Prefecture, Huili, Sichuan, China.
  • 2 Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China.
PMID: 41701749 DOI: 10.1371/journal.pone.0343053
Abstract

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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