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TRIM11 通过 UBE2N-TAX1BP1 信号通路防止哮喘模型中的铁死亡。

TRIM11 Prevents Ferroptosis in model of asthma by UBE2N-TAX1BP1 signaling.

机构信息

Department of Respiratory and Critical Care Medicine, Longgang Central Hospital, 6082 Longgang Avenue, Shenzhen, 518116, China.

出版信息

BMC Pulm Med. 2024 Oct 29;24(1):542. doi: 10.1186/s12890-024-03351-9.


DOI:10.1186/s12890-024-03351-9
PMID:39472837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11523820/
Abstract

Asthma is a complex chronic respiratory inflammatory disease affected by both genetic and environmental factors. Therefore, our study explored the influence of TRIM11 on asthma and its underlying mechanisms. Our research involved patients diagnosed with asthma and healthy volunteers recruited from our hospital. We observed a reduction in serum TRIM11 expression in asthma patients, which positively correlated with the levels of anti-IgE or IgE. Additionally, both TRIM11 mRNA and protein expression in lung tissue were diminished. The introduction of the TRIM11 gene resulted in a reduction in inflammation in an in vitro asthma model and prevented the development of asthma in a mouse model. Moreover, the TRIM11 gene exhibited a suppressive effect on Ferroptosis and mitigated ROS-induced mitochondrial damage in the asthma model. TRIM11 was found to stimulate UBE2N-TAX1BP1 signaling in the asthma model, with UBE2N being identified as the specific target for TRIM11's effects on Ferroptosis. Furthermore, TRIM11 protein interacted with UBE2N protein and facilitated the dissociation of UBE2N-UBE2N in the asthma model. In conclusion, TRIM11 plays a vital role in preventing Ferroptosis in the asthma model through UBE2N-TAX1BP1 signaling. This indicates that targeting the TRIM11 mechanism could serve as a promising strategy for anti-Ferroptosis immunotherapy in asthma treatment.

摘要

哮喘是一种复杂的慢性呼吸道炎症性疾病,受遗传和环境因素的影响。因此,我们的研究探讨了 TRIM11 对哮喘的影响及其潜在机制。我们的研究涉及在我院确诊的哮喘患者和健康志愿者。我们观察到哮喘患者血清中 TRIM11 表达降低,且与抗 IgE 或 IgE 水平呈正相关。此外,肺组织中 TRIM11 mRNA 和蛋白表达均减少。在体外哮喘模型中引入 TRIM11 基因可减少炎症反应,并可预防哮喘在小鼠模型中的发生。此外,TRIM11 基因对哮喘模型中的 Ferroptosis 具有抑制作用,并减轻了 ROS 诱导的线粒体损伤。研究发现 TRIM11 在哮喘模型中刺激 UBE2N-TAX1BP1 信号通路,UBE2N 是 TRIM11 对 Ferroptosis 作用的特异性靶点。此外,TRIM11 蛋白与 UBE2N 蛋白相互作用,并促进哮喘模型中 UBE2N-UBE2N 的解离。总之,TRIM11 通过 UBE2N-TAX1BP1 信号通路在哮喘模型中发挥重要作用,防止 Ferroptosis。这表明针对 TRIM11 机制可能成为哮喘治疗中抗 Ferroptosis 免疫治疗的一种有前途的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/ece173f5a016/12890_2024_3351_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/8e581060f245/12890_2024_3351_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/e8755e1bc0f7/12890_2024_3351_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/6113d00f4598/12890_2024_3351_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/ab00609a763c/12890_2024_3351_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/bc8d9040dcca/12890_2024_3351_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/b38287d8b4ea/12890_2024_3351_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/e10d8afbdb5d/12890_2024_3351_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/560933609292/12890_2024_3351_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/c37c930abac5/12890_2024_3351_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/ece173f5a016/12890_2024_3351_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/8e581060f245/12890_2024_3351_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/e8755e1bc0f7/12890_2024_3351_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/6113d00f4598/12890_2024_3351_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/ab00609a763c/12890_2024_3351_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/bc8d9040dcca/12890_2024_3351_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/b38287d8b4ea/12890_2024_3351_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/e10d8afbdb5d/12890_2024_3351_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/560933609292/12890_2024_3351_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/c37c930abac5/12890_2024_3351_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc0a/11523820/ece173f5a016/12890_2024_3351_Fig10_HTML.jpg

相似文献

[1]
TRIM11 Prevents Ferroptosis in model of asthma by UBE2N-TAX1BP1 signaling.

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[4]
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[5]
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[6]
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[7]
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[8]
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[10]
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本文引用的文献

[1]
Apolipoprotein C3 (ApoC3) facilitates NLRP3 mediated pyroptosis of macrophages through mitochondrial damage by accelerating of the interaction between SCIMP and SYK pathway in acute lung injury.

Int Immunopharmacol. 2024-2-15

[2]
A Study of the Relationship between Phthalate Exposure and the Occurrence of Adult Asthma in Taiwan.

Molecules. 2023-7-5

[3]
Beneficial Effects of (Fisch.) Bunge Extract in Controlling Inflammatory Response and Preventing Asthma Features.

Int J Mol Sci. 2023-6-30

[4]
Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.

Int J Mol Sci. 2023-6-21

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J Clin Med. 2023-6-29

[6]
Benralizumab in Patients with Severe Eosinophilic Asthma: A Multicentre Real-Life Experience.

J Clin Med. 2023-6-28

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

J Inflamm Res. 2023-7-1

[8]
TRIM11 expression in non-small cell lung cancer is associated with poor prognosis.

Histol Histopathol. 2024-4

[9]
TRIM11 Posttranscriptionally Modulated by miR-5193 Facilitates Tumor Growth and Metastasis of Prostate Cancer.

Technol Cancer Res Treat. 2023

[10]
Ferroptosis participates in dibutyl phthalate-aggravated allergic asthma in ovalbumin-sensitized mice.

Ecotoxicol Environ Saf. 2023-5

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