IL-13 facilitates ferroptotic death in asthmatic epithelial cells via SOCS1-mediated ubiquitinated degradation of SLC7A11

Miao, Manli; Pan, Min; Chen, Xu; Shen, Jiapan; Zhang, Ling; Feng, Xiaoxia; Chen, Mengting; Cui, Guofeng; Zong, Huaiyuan; Zhang, Wen; Chang, Shuang; Xu, Fangzhou; Wang, Zixi; Li, Dapeng; Liu, Weiwei; Ding, Zhao; Zhang, Shengquan; Chen, Biao; Zha, Xiaojun; Fan, Xiaoyun

doi:10.1016/j.redox.2024.103100

Cited by 3 publications

(1 citation statement)

References 62 publications

(74 reference statements)

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“…61 The E3 ubiquitin ligase SOCS1 binds to and catalyses the ubiquitinated degradation of SLC7A11, thereby promoting ferroptosis in airway epithelial cells. 62 SLC7A11 may play a role in the pathogenesis of pulmonary fibrosis by regulating redox balance, attenuating oxidative damage and modulating mechanisms associated with inflammation. 24,63 Chronic lung disease itself is not a cause of lung cancer, but individuals with chronic lung disease may have an increased risk of developing lung cancer.…”

Section: Glutamate Metabolism In Chronic Lung Diseasesmentioning

confidence: 99%

Targeting glutamate metabolism in chronic lung diseases

Guo,

Yan

2024

Clinical and Translational Dis

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Amino acids are necessary for all life forms, which play various roles. Disorder of amino acid metabolism is now considered an important driving mechanism in diverse pulmonary conditions, particularly chronic lung diseases like chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and lung cancer. Glutamate actively participates in multiple vital biological processes, while the intricate glutamate metabolism, glutamate receptors and glutamate transporters assume crucial regulatory functions in the development of chronic lung diseases. This review aims to discuss the relationship between glutamate dysfunction and chronic lung diseases. By discussing the physiological and pathological function of glutamate, we probe the potential drug targets for chronic lung diseases in the glutamate pathway.

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Section: Glutamate Metabolism In Chronic Lung Diseasesmentioning

confidence: 99%

Targeting glutamate metabolism in chronic lung diseases

Guo,

Yan

2024

Clinical and Translational Dis

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Au/FeNiPO₄‐Based Multiple Spectra Optoacoustic Tomography/CT Dual‐Mode Nanoprobe for Systemic Screening of Atherosclerotic Vulnerable Plaque

Cai,

Ge,

et al. 2024

Adv Funct Materials

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Current diagnostic technique in direct identification of multi‐site plaques and simultaneous assessment of plaque vulnerability remains a challenge, which is crucial for indicating the risk of atherosclerotic cardiovascular diseases (ASCVD). Herein, an osteopontin (OPN)‐specific nanoprobe (OPN Ab‐Au/FeNiPO4@ICG) with both multiple spectra optoacoustic tomography (MSOT) and computed tomography (CT) imaging, is constructed successfully realizing systemic screening of vulnerable plaque. OPN Ab‐Au/FeNiPO4@ICG nanoprobe specifically targeted OPN‐overexpressed foam cells and recognized the vulnerable plaque at the molecular level. In AS mice, CT imaging exhibits that OPN Ab‐Au/FeNiPO4@ICG nanoprobe effectively avoid interference from calcification and accurately visualized AS plaque. MSOT functional imaging results reveals that after the injection of OPN Ab‐Au/FeNiPO4@ICG nanoprobe, the carotid plaque exhibited a much higher MSOT signal than the aortic arch plaque (P = 0.0291). Further pathological analysis displays that the carotid plaque possessed a much higher vulnerability score (P = 0.0247), in agreement with the MSOT signals. More importantly, the linear regression analysis confirms the high correlation between the MSOT signals and plaque vulnerability with R = 0.7095 (P = 0.0216), demonstrating the potential of the proposed nanoprobe in systematic evaluation of plaque vulnerability. This work employs the dual‐model nanoprobe strategy for both plaque localization and vulnerability assessment, greatly advancing the accurate diagnosis of ASCVD.

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ETS1 and RBPJ transcriptionally regulate METTL14 to suppress TGF-β1-induced epithelial-mesenchymal transition in human bronchial epithelial cells

Chen,

Li,

Yuan

et al. 2024

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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IL-13 facilitates ferroptotic death in asthmatic epithelial cells via SOCS1-mediated ubiquitinated degradation of SLC7A11

Cited by 3 publications

References 62 publications

Targeting glutamate metabolism in chronic lung diseases

Targeting glutamate metabolism in chronic lung diseases

Au/FeNiPO₄‐Based Multiple Spectra Optoacoustic Tomography/CT Dual‐Mode Nanoprobe for Systemic Screening of Atherosclerotic Vulnerable Plaque

ETS1 and RBPJ transcriptionally regulate METTL14 to suppress TGF-β1-induced epithelial-mesenchymal transition in human bronchial epithelial cells

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IL-13 facilitates ferroptotic death in asthmatic epithelial cells via SOCS1-mediated ubiquitinated degradation of SLC7A11

Cited by 3 publications

References 62 publications

Targeting glutamate metabolism in chronic lung diseases

Targeting glutamate metabolism in chronic lung diseases

Au/FeNiPO4‐Based Multiple Spectra Optoacoustic Tomography/CT Dual‐Mode Nanoprobe for Systemic Screening of Atherosclerotic Vulnerable Plaque

ETS1 and RBPJ transcriptionally regulate METTL14 to suppress TGF-β1-induced epithelial-mesenchymal transition in human bronchial epithelial cells

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Product

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About

Au/FeNiPO₄‐Based Multiple Spectra Optoacoustic Tomography/CT Dual‐Mode Nanoprobe for Systemic Screening of Atherosclerotic Vulnerable Plaque