职业性哮喘（OA）是一种常见的职业性肺部疾病，经常被诊断不足和报告不足。诊断和治疗骨关节炎的复杂性造成了巨大的社会和经济负担，使其成为一个重要的公共卫生问题。除了避免过敏原外，骨关节炎患者还需要药物治疗；然而，新的治疗靶点和策略需要进一步研究。自噬可能是一个有前景的干预目标，但缺乏总结自噬在 OA 中作用的相关研究。这篇综述巩固了目前对 OA 的理解，详细介绍了导致其发生的主要和新的药物。此外，我们总结了HMW和LMW制剂诱导OA中的自噬机制，揭示职业过敏原可诱导肺上皮细胞、平滑肌细胞和树突状细胞自噬紊乱，最终通过炎症反应、氧化应激和炎症反应导致OA。细胞死亡。最后，我们讨论了将自噬作为治疗 OA 甚至类固醇抵抗性哮喘的有效策略的前景，包括针对类器官、芯片器官系统、纳米材料载体和纳米气泡的自噬干预措施；开发组合暴露模型，以及非经典自噬在职业性哮喘中的作用。简而言之，这篇综述总结了自噬在职业性哮喘中的作用，为基于自噬的 OA 干预提供了理论基础，并确定了未来研究的方向和挑战。版权所有 © 2024。由 Elsevier B.V. 出版。

Occupational asthma (OA) is a common occupational pulmonary disease that is frequently underdiagnosed and underreported. The complexity of diagnosing and treating OA creates a significant social and economic burden, making it an important public health issue. In addition to avoiding allergens, patients with OA require pharmacotherapy; however, new therapeutic targets and strategies need further investigation. Autophagy may be a promising intervention target, but there is a lack of relevant studies summarizing the role of autophagy in OA. In this review consolidates the current understanding of OA, detailing principal and novel agents responsible for its onset. Additionally, we summarize the mechanisms of autophagy in HMW and LMW agents induced OA, revealing that occupational allergens can induce autophagy disorders in lung epithelial cells, smooth muscle cells, and dendritic cells, ultimately leading to OA through involving inflammatory responses, oxidative stress, and cell death. Finally, we discuss the prospects of targeting autophagy as an effective strategy for managing OA and even steroid-resistant asthma, encompassing autophagy interventions focused on organoids, organ-on-a-chip systems, nanomaterials vehicle, and nanobubbles; developing combined exposure models, and the role of non-classical autophagy in occupational asthma. In briefly, this review summarizes the role of autophagy in occupational asthma, offers a theoretical foundation for OA interventions based on autophagy, and identifies directions and challenges for future research.Copyright © 2024. Published by Elsevier B.V.