Programmed Cell Death in Asthma: Apoptosis, Autophagy, Pyroptosis, Ferroptosis, and Necroptosis

Bronchial asthma is a complex heterogeneous airway disease, which has emerged as a global health issue. A comprehensive understanding of the different molecular mechanisms of bronchial asthma may be an efficient means to improve its clinical efficacy in the future. Increasing research evidence indicates that some types of programmed cell death (PCD), including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis, contributed to asthma pathogenesis, and may become new targets for future asthma treatment. This review briefly discusses the molecular mechanism and signaling pathway of these forms of PCD focuses on summarizing their roles in the pathogenesis and treatment strategies of asthma and offers some efficient means to improve clinical efficacy of therapeutics for asthma in the near future.

Automated summary

Bronchial asthma, a complex heterogeneous airway disease, has become a global health issue. Understanding the different molecular mechanisms of asthma could improve clinical efficacy. Evidence suggests that various forms of programmed cell death (PCD) contribute to asthma pathogenesis and may be potential targets for future asthma treatment. This review discusses the molecular mechanisms and signaling pathways of PCD, summarizes their roles in asthma pathogenesis and treatment, and offers potential means to enhance clinical efficacy.