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

Abstract

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.

Keywords:

• asthma
• bronchial asthma
• programmed cell death

Acknowledgments

This work was supported by the National Natural Science Foundation of China, 82270104.This study was supported by “the Fundamental Research Funds for the Central Universities” (2042023kf0044).

Author Contributions

Huo-Jun Zhang and Hui-Guo Liu contributed to the conception of the study. Lu Liu drafted the manuscript under the help of Ling Zhou. Lingling Wang and Peng-Dou Zheng, Feng-Qin Zhang and Zhen-Yu Mao took part in drafting, revising or critically reviewing the article. All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare no conflicts of interest in this work.