ArticleBMC pulmonary medicine2022
The role of ferroptosis in chronic intermittent hypoxia-induced lung injury.
Article in BMC pulmonary medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Lung Vascular Remodeling and Oxidative Damage Induced by Chronic Intermittent Hypoxia.International journal of molecular sciences · 2026Article
- Paeoniflorin alleviates hypobaric hypoxia-triggered lung injury through targeting MEK2 to modulate ERK2-SGK1 signaling.Acta pharmaceutica Sinica. B · 2026Article
- Dimethyl fumarate alleviates inflammation during high altitude hypoxia induced acute lung injury by upregulating Nrf2/SLC7A11 pathway in ferroptosis.Clinical proteomics · 2025Article
- Role of Ferroptosis on Lung Epithelial Cells in Disease Progression and Treatment: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Article
- Programmed cell death in the cognitive impairment of obstructive sleep apnea.Cell & bioscience · 2025Review
- 2-Methoxyestradiol attenuates lung injury induced by chronic intermittent hypoxia via inhibiting the HIF1-α/SLC7A11 pathway.Scientific reports · 2025Article
- Ferroptosis as a Potential Mechanism in the Pathophysiology of Obstructive Sleep Apnea Syndrome.Nature and science of sleep · 2025Review
- Ferroptosis: a key driver and therapeutic target in the pathogenesis of acute respiratory distress syndrome.Frontiers in immunology · 2025Review
- Iron Overload-induced Ferroptosis as a Target for Protection against Obliterative Bronchiolitis after Orthotopic Tracheal Transplantation in Mice.Current molecular medicine · 2025Article
- Carvedilol Confers Ferroptosis Resistance in HL-1 Cells by Upregulating GPX4, FTH1, and FTL1 and Inducing Metabolic Remodeling Under Hypoxia/Reoxygenation.Antioxidants (Basel, Switzerland) · 2024Article
- Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges.Cell death discovery · 2024Review
- 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol) alleviates lung injury by inhibiting SIRT6-HIF-1α signaling pathway activation through the upregulation of miR-212-5p expression.Molecular biology reports · 2024Article
- Ferrostatin-1 Reversed Chronic Intermittent Hypoxia-Induced Ferroptosis in Aortic Endothelial Cells via Reprogramming Mitochondrial Function.Nature and science of sleep · 2024Article
- Ferroptosis Regulated by Hypoxia in Cells.Cells · 2023Review
- Ferroptosis-related genes are considered as potential targets for CPAP treatment of obstructive sleep apnea.Frontiers in neurology · 2023Article
- Article
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Authors and funding
8 authors.
Funding
Abstract
purposeChronic intermittent hypoxia (CIH) causes lung injury but the mechanism is unclear. Ferroptosis is a novel form of programmed cell death. In this research, we attempted to explore the role of ferroptosis in CIH-induced lung injury both in vitro and in vivo.
methodsSprague-Dawley rats were randomly separated into control group, CIH group and CIH + ferrostatin-1 group (CIH + Fer-1). Rats in the CIH group and CIH + Fer-1 group were exposed to intermittent hypoxia for 12 weeks. Human bronchial epithelial cell line (BEAS-2B) was cultivated for 24 h in either conventional culture medium or under CIH conditions. Fer-1 was applied to observe its treatment effects. Histological changes were evaluated by Hematoxylin-eosin (HE) staining and masson staining. The expression levels of Acyl-CoA synthetase long-chain family member 4 (ACSL4), glutathione peroxidase 4 (GPX4), interleukin-6 (IL-6) and tumour necrosis factor α (TNFα) were detected via qRT-PCR or Western blot. Cell counting kit-8 (CCK-8) was used to assess cell viability. The apoptotic rate and reactive oxygen species (ROS) was calculated by flow cytometry.
resultsHistology showed that CIH treatment induced lung injury and pulmonary fibrosis in lung tissue. After Fer-1 treatment, the pathological changes caused by CIH alleviated. The mRNA and protein levels of GPX4 decreased significantly in lung tissues of CIH-treated rats and BEAS-2B, (p < 0.05). The mRNA and protein levels of ACSL4 increased significantly in lung tissues of CIH-treated rats and BEAS-2B, (p < 0.05). The mRNA levels of IL-6 and TNFα in BEAS-2B increased after CIH treatment, (p < 0.05). Cell viability decreased, apoptosis rate and ROS increased in CIH-treated BEAS-2B, (p < 0.05). Cotreatment with Fer-1 reversed CIH-induced apoptosis, cell viability, ROS accumulation, mRNA and protein levels of GPX4, ACSL4, IL-6 and TNFα both in vitro and in vivo (p < 0.05).
conclusionsFerroptosis occurred in CIH-induced lung injury, both in vitro and in vivo. The ferroptosis inhibitor Fer-1 alleviated cell injury and ferroptosis in CIH-treated BEAS-2B and lung tissues of rats.
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