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Hypoxia: a critical pathophysiological driver in respiratory inflammatory diseases
Bing Zhong1,2, Lan Yang3, Si-Lu Sun4
1Department of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
Military Medical Research
|May 1, 2026
Summary
Hypoxia, driven by hypoxia-inducible factor 1α (HIF-1α), worsens inflammatory airway diseases by damaging barriers, altering immune responses, and accelerating remodeling. Targeting HIF-1α offers a unified approach for developing precise therapies.
Area of Science:
- Pulmonary Medicine
- Immunology
- Cellular Biology
Background:
- Hypoxia is a key factor in inflammatory airway diseases like asthma and COPD.
- Hypoxia-inducible factor 1α (HIF-1α) signaling is a central mechanism driving disease progression.
- Shared pathophysiological pathways exist across different inflammatory airway diseases due to hypoxia.
Purpose of the Study:
- To synthesize hypoxia-driven mechanisms common to inflammatory airway diseases.
- To establish a unifying framework for HIF-1α signaling in these diseases.
- To highlight therapeutic implications and guide the development of targeted interventions.
Main Methods:
- This review synthesizes existing literature on hypoxia and HIF-1α signaling in airway diseases.
- It analyzes shared mechanisms of hypoxia-induced inflammation and tissue remodeling.
- The study provides a cross-disease perspective on hypoxia pathways.
Main Results:
- Hypoxia, via HIF-1α, disrupts epithelial integrity and initiates inflammation.
- HIF-1α reprograms immune cells (eosinophils, T cells, macrophages) and alters cytokine profiles.
- Hypoxia accelerates airway remodeling, leading to airflow limitation and persistent inflammation.
Conclusions:
- Targeting HIF-1α is crucial for developing effective therapies for inflammatory airway diseases.
- Disease-tailored interventions are needed, considering distinct pathological features.
- Further translational and clinical research on hypoxia is essential to build an evidence base for practice.
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