Skip to content
DraconiticResearch
Search Sources API
194,067 studies31 sourcesUpdated 48 min ago
Peer-reviewedCC BY 4.0Biomedicine Hub

Targeting Endoplasmic Reticulum Stress with Tauroursodeoxycholic Acid: A Potential Therapeutic Strategy for Allergic Airway Diseases

  1. 1School of Medicine, The Chinese University of Hong Kong, Shenzhen, China

Abstract

Background: Allergic airway diseases (AADs) such as asthma and allergic rhinitis impose a heavy global health burden, characterized by chronic airway inflammation, airway hyperresponsiveness, and structural remodeling. Endoplasmic reticulum (ER) stress has been increasingly identified as a key driver of AAD pathogenesis. As a well-characterized chemical chaperone, tauroursodeoxycholic acid (TUDCA) exhibits promising therapeutic potential for AADs by regulating immunity, relieving inflammation, and reversing airway pathological lesions.

Summary: This review summarizes how ER stress drives AAD development and progression of AADs and details the molecular mechanisms underlying the therapeutic effects of TUDCA by targeting ER stress-related unfolded protein response signaling pathways. Additionally, it highlights preclinical evidence supporting the efficacy of TUDCA and discusses the prospects and challenges associated with its clinical translation.

Key Messages: ER stress is a key pathogenic factor in AADs; TUDCA can target ER stress-related signaling pathways to exert therapeutic effects on AADs; preclinical studies confirm the efficacy of TUDCA, and its clinical translation may provide a novel ER stress-targeted strategy to optimize AAD management and improve patient outcomes.

Related

  1. Mechanisms and therapeutic prospects of short-chain fatty acids in neonatal hypoxic–ischemic encephalopathy via modulation of mitochondrial dysfunction and endoplasmic reticulum stress
    Yinyu Wang, Lingjuan Gao, Yu Xu +5
    Frontiers in Molecular NeurosciencePeer-reviewedCC BY 4.0Full textObstetrics, gynaecology & paediatricsPMCEurope PMC
  2. Targeting Endoplasmic Reticulum Stress With Exogenous GDNF Promotes Diabetic Corneal Epithelial and Neural Repair via PI3K/AKT Signaling.
    Haoyu Li, Jianfeng Long, Shirui Dai +3
    Investigative ophthalmology & visual sciencePeer-reviewedCC BY-NC-NDFull textMedical imaging & radiologyEurope PMC
  3. Hepatoprotective mechanism of tauroursodeoxycholic acid and its therapeutic potential in liver diseases
    Ruting Chao, Yanan Zhang, Yuanzhu Hao +3
    Frontiers in PharmacologyPeer-reviewedCC BY 4.0Full textPharmacology & toxicologyCrossrefDOAJ
  4. PRKACA modulates endoplasmic reticulum stress-associated dysfunction in granulosa cell models relevant to polycystic ovary syndrome
    Yan Zhang, Meihuan Chen, Yuan Lin +3
    Scientific ReportsPeer-reviewedCC BY-NC-ND 4.0Full textObstetrics, gynaecology & paediatricsCrossref
  5. Polycystin-2 functions as a calcium leak channel under endoplasmic reticulum stress to protect against myocardial ischemia
    Virdjinija Vuchkovska, Sanjeet Paluru, Ryne M. Knutila +6
    Cell ReportsPeer-reviewedCC BY-NC-ND 4.0General medicineCrossref
BibTeX
@article{han2026targeting,
  title = {{Targeting Endoplasmic Reticulum Stress with Tauroursodeoxycholic Acid: A Potential Therapeutic Strategy for Allergic Airway Diseases}},
  author = {Yining Han},
  journal = {Biomedicine Hub},
  year = {2026},
  month = oct,
  doi = {10.1159/bmh/aboag006},
  url = {https://doi.org/10.1159/bmh/aboag006},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Targeting Endoplasmic Reticulum Stress with Tauroursodeoxycholic Acid: A Potential Therapeutic Strategy for Allergic Airway Diseases
AU  - Yining Han
PY  - 2026
DA  - 2026/10/10
JO  - Biomedicine Hub
DO  - 10.1159/bmh/aboag006
UR  - https://doi.org/10.1159/bmh/aboag006
AB  - Background: Allergic airway diseases (AADs) such as asthma and allergic rhinitis impose a heavy global health burden, characterized by chronic airway inflammation, airway hyperresponsiveness, and structural remodeling. Endoplasmic reticulum (ER) stress has been increasingly identified as a key driver of AAD pathogenesis. As a well-characterized chemical chaperone, tauroursodeoxycholic acid (TUDCA) exhibits promising therapeutic potential for AADs by regulating immunity, relieving inflammation, and reversing airway pathological lesions.  Summary: This review summarizes how ER stress drives AAD development and progression of AADs and details the molecular mechanisms underlying the therapeutic effects of TUDCA by targeting ER stress-related unfolded protein response signaling pathways. Additionally, it highlights preclinical evidence supporting the efficacy of TUDCA and discusses the prospects and challenges associated with its clinical translation.  Key Messages: ER stress is a key pathogenic factor in AADs; TUDCA can target ER stress-related signaling pathways to exert therapeutic effects on AADs; preclinical studies confirm the efficacy of TUDCA, and its clinical translation may provide a novel ER stress-targeted strategy to optimize AAD management and improve patient outcomes.
SN  - 2296-6870
ER  -