Department of Pulmonary and Critical Care Medicine, First Affiliated Hospital, Kunming Medical University, Kunming, China.
Pediatric Medicine Class One, Kunming Medical University, Kunming, China.
Ther Adv Respir Dis. 2023 Jan-Dec;17:17534666231208628. doi: 10.1177/17534666231208628.
Ferroptosis is a regulatory cell death characterized by intracellular iron accumulation and lipid peroxidation that leads to oxidative stress. Many signaling pathways such as iron metabolism, lipid metabolism, and amino acid metabolism precisely regulate the process of ferroptosis. Ferroptosis is involved in a variety of lung diseases, such as acute lung injury, chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis. Increasing studies suggest that ferroptosis is involved in the development of asthma. Ferroptosis plays an important role in asthma. Iron metabolism disorders, lipid peroxidation, amino acid metabolism disorders lead to the occurrence of ferroptosis in airway epithelial cells, and then aggravate clinical symptoms in asthmatic patients. Moreover, several regulators of ferroptosis are involved in the pathogenesis of asthma, such as Nrf2, heme oxygenase-1, mevalonate pathway, and ferroptosis inhibitor protein 1. Importantly, ferroptosis inhibitors improve asthma. Thus, the pathogenesis of ferroptosis and its contribution to the pathogenesis of asthma help us better understand the occurrence and development of asthma, and provide new directions in asthma treatment. This article aimed to review the role and mechanism of ferroptosis in asthma, describing the relationship between ferroptosis and asthma based on signaling pathways and related regulatory factors. At the same time, we summarized current observations of ferroptosis in eosinophils, airway epithelial cells, and airway smooth muscle cells in asthmatic patients.
铁死亡是一种受调控的细胞死亡方式，其特征是细胞内铁积累和脂质过氧化，导致氧化应激。许多信号通路，如铁代谢、脂质代谢和氨基酸代谢，精确地调节铁死亡的过程。铁死亡参与多种肺部疾病，如急性肺损伤、慢性阻塞性肺疾病（COPD）和肺纤维化。越来越多的研究表明，铁死亡参与了哮喘的发生。铁死亡在哮喘中起重要作用。铁代谢紊乱、脂质过氧化、氨基酸代谢紊乱导致气道上皮细胞发生铁死亡，进而加重哮喘患者的临床症状。此外，几种铁死亡调节剂参与了哮喘的发病机制，如 Nrf2、血红素加氧酶-1、甲羟戊酸途径和铁死亡抑制剂蛋白 1。重要的是，铁死亡抑制剂改善了哮喘。因此，铁死亡的发病机制及其对哮喘发病机制的贡献有助于我们更好地理解哮喘的发生和发展，并为哮喘治疗提供新的方向。本文旨在综述铁死亡在哮喘中的作用和机制，根据信号通路和相关调节因子描述铁死亡与哮喘的关系。同时，我们总结了目前在哮喘患者的嗜酸性粒细胞、气道上皮细胞和气道平滑肌细胞中观察到的铁死亡情况。
