Identification and validation of ferroptosis-related genes in lipopolysaccharide-induced acute lung injury

Wang, Sijiao; Song, Yansha; Xu, Fan; Liu, Han Han; Shen, Yue; Hu, Lijuan; Fu, Yi‐Peng; Zhu, Lei

doi:10.1016/j.cellsig.2023.110698

Cited by 5 publications

(3 citation statements)

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“…Recent studies have suggested that ferroptosis plays an important role in lung disease, pulmonary hypoxic injury, and pneumonia (Xu et al 2021 ). Study have confirmed the role of ferroptosis-related genes in lipopolysaccharide-induced acute lung injury (Wang et al 2023 ). In human coronavirus disease 2019 induced ALI, ferroptosis was also observed in human cardiac and lung tissue (Jacobs et al 2020 ).…”

Section: Discussionmentioning

confidence: 68%

Meteorin-like/Meteorin-β protects LPS-induced acute lung injury by activating SIRT1-P53-SLC7A11 mediated ferroptosis pathway

Chen,

Li,

Peng

et al. 2023

Mol Med

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Background Ferroptosis plays an essential role in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Meteorin-like/Meteorin-β (Metrnβ) is a protein secreted by skeletal muscle and adipose tissue and plays a role in cardiovascular diseases. However, its role in acute lung injury has not been elucidated. Methods In this study, we used an adenovirus (Ad) delivery system to overexpress or knockdown Metrnβ in lung tissue to examine the role of Metrnβ in LPS-induced acute lung injury. Results We found that ferroptosis was increased during LPS-induced ALI. The expression of Metrnβ was reduced in ALI lung tissue. Overexpression of Metrnβ in lung tissue alleviated LPS-induced lung injury, inflammation, and ferroptosis. Moreover, Metrnβ knockout in lung tissue accelerated LPS-induced ALI, inflammation, and ferroptosis. We also cultured MLE-12 cells and transfected the cells with Ad-Metrnβ or Metrnβ siRNA. Metrnβ overexpression ameliorated LPS-induced MLE cell death, inflammation and ferroptosis, while Metrnβ knockdown aggregated cell survival and decreased inflammation and ferroptosis. Moreover, we found that Metrnβ enhanced ferroptosis-related Gpx4 expression and reduced ferroportin and ferritin levels. Furthermore, we found that Metrnβ positively regulated SIRT1 transcription thus inhibited P53, increased SLC7A11 expression. When we used the ferroptosis inhibitor ferrostatin-1, the deteriorating effects of Metrnβ knockout were abolished in ALI mice. Moreover, SIRT1 knockout also abolished the protective effects of Metrnβ overexpression in vivo. Conclusions Taken together, Metrnβ could protect LPS-induced ALI by activating SIRT1-P53- SLC7A11 mediated ferroptosis inhibition.

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Section: Discussionmentioning

confidence: 68%

Meteorin-like/Meteorin-β protects LPS-induced acute lung injury by activating SIRT1-P53-SLC7A11 mediated ferroptosis pathway

Chen,

Li,

Peng

et al. 2023

Mol Med

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Section: Ferroptosis In Respiratory Diseasesmentioning

confidence: 99%

“…106 In addition, ferroptosis seems to play a role in LPS-induced ALI, as reflected in the increased levels of MDA, 4-HNE and total iron as well as the decreased expression of SLC7A11 and GPX4 in both an animal model of ALI and in a bronchial epithelial cell line stimulated with lipopolysaccharide (LPS). 107 As ALI progresses to ARDS, neutrophils and their substances, including oxidants, proteolytic hydrolases, plateletactivating factors and leukotrienes, become increasingly important in the pathological development of ARDS by negatively impacting the alveolar-capillary membranes. In turn, the disruption and balance of endogenous antiproteases, antioxidants and anti-inflammatory cytokines determine the extent of tissue damage and the severity of clinical symptoms.…”

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confidence: 99%

Unraveling the Molecular Regulation of Ferroptosis in Respiratory Diseases

Zhu,

Zhou,

et al. 2024

JIR

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Ferroptosis, a type of programmed cell death that relies on iron, is distinct in terms of its morphological, biochemical and genetic features. Unlike other forms of cell death, such as autophagy, apoptosis, necrosis, and pyroptosis, ferroptosis is primarily caused by lipid peroxidation. Cells that die due to iron can potentially trigger an immune response which intensifies inflammation and causes severe inflammatory reactions that eventually lead to multiple organ failure. In recent years, ferroptosis has been identified in an increasing number of medical fields, including neurological pathologies, chronic liver diseases and sepsis. Ferroptosis has the potential to cause an inflammatory tempest, with many of the catalysts and pathological indications of respiratory ailments being linked to inflammatory reactions. The growing investigation into ferroptosis in respiratory disorders has also garnered significant interest to better understand the mechanism of ferroptosis in these diseases. In this review, the recent progress in understanding the molecular control of ferroptosis and its mechanism in different respiratory disorders is examined. In addition, this review discusses current challenges and prospects for understanding the link between respiratory diseases and ferroptosis.

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