Scholarlink

<p>Asthma is a major chronic non-communicable respiratory disease, affecting over 300 million individuals globally, with an adult prevalence of 4.3%. Despite advances in individualized treatment, a subset of patients, particularly those with non-type 2 (non-T2) asthma, fails to achieve optimal disease control. Non-T2 asthma, characterized by steroid resistance and heterogeneous immune responses, remains a therapeutic challenge. Emerging evidence suggests that circadian rhythm disruption may modulate key pathological processes relevant to non-T2 asthma, including immune imbalance, epithelial barrier dysfunction, and impaired glucocorticoid sensitivity. This review investigates evidence of an association between circadian clock dysfunction and non-type 2 asthma pathogenesis, and proposes a hypothesis-driven framework to guide future studies. Chronotherapeutic strategies and clock-targeted interventions may offer promising avenues for future research and individualized treatment.</p> Graphical Abstract <p>Integrated model linking circadian clock disruption to the pathogenesis of non-T2 asthma</p> <p>Disruption of the circadian clock alters immune homeostasis, promoting NEU inflammation, epithelial dysfunction, and steroid resistance—hallmarks of non-type 2 asthma. Key circadian regulators (BMAL1, REV-ERBα, RORs, CRYs, and PERs) modulate inflammatory cytokines and immune cell polarization, which may act as a potential upstream driver in the development and persistence of non-type 2 asthma.</p> <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Circadian Clock Disruption and Non-type 2 Asthma: A Hypothesis-Driven Perspective on Immune, Epithelial, and Steroid Response

  • 期刊论文

  • 发表日期：

    2025年7月25日

查看全文
  • Haohua Huang,
  • Xiaoxiao Jiang,
  • Qian Du,
  • Hua Liao,
  • Shaoxi Cai,
  • Hangming Dong

摘要

Asthma is a major chronic non-communicable respiratory disease, affecting over 300 million individuals globally, with an adult prevalence of 4.3%. Despite advances in individualized treatment, a subset of patients, particularly those with non-type 2 (non-T2) asthma, fails to achieve optimal disease control. Non-T2 asthma, characterized by steroid resistance and heterogeneous immune responses, remains a therapeutic challenge. Emerging evidence suggests that circadian rhythm disruption may modulate key pathological processes relevant to non-T2 asthma, including immune imbalance, epithelial barrier dysfunction, and impaired glucocorticoid sensitivity. This review investigates evidence of an association between circadian clock dysfunction and non-type 2 asthma pathogenesis, and proposes a hypothesis-driven framework to guide future studies. Chronotherapeutic strategies and clock-targeted interventions may offer promising avenues for future research and individualized treatment.

Graphical Abstract

Integrated model linking circadian clock disruption to the pathogenesis of non-T2 asthma

Disruption of the circadian clock alters immune homeostasis, promoting NEU inflammation, epithelial dysfunction, and steroid resistance—hallmarks of non-type 2 asthma. Key circadian regulators (BMAL1, REV-ERBα, RORs, CRYs, and PERs) modulate inflammatory cytokines and immune cell polarization, which may act as a potential upstream driver in the development and persistence of non-type 2 asthma.