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抑制肺微生物群衍生的促凋亡肽可改善肺纤维化的急性加重。

Inhibition of lung microbiota-derived proapoptotic peptides ameliorates acute exacerbation of pulmonary fibrosis.

机构信息

Department of Immunology, Mie University Faculty and Graduate School of Medicine, Tsu, Mie, Japan.

Center for Intractable Diseases, Mie University, Tsu, Mie, Japan.

出版信息

Nat Commun. 2022 Mar 23;13(1):1558. doi: 10.1038/s41467-022-29064-3.

DOI:10.1038/s41467-022-29064-3
PMID:35322016
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8943153/
Abstract

Idiopathic pulmonary fibrosis is an incurable disease of unknown etiology. Acute exacerbation of idiopathic pulmonary fibrosis is associated with high mortality. Excessive apoptosis of lung epithelial cells occurs in pulmonary fibrosis acute exacerbation. We recently identified corisin, a proapoptotic peptide that triggers acute exacerbation of pulmonary fibrosis. Here, we provide insights into the mechanism underlying the processing and release of corisin. Furthermore, we demonstrate that an anticorisin monoclonal antibody ameliorates lung fibrosis by significantly inhibiting acute exacerbation in the human transforming growth factorβ1 model and acute lung injury in the bleomycin model. By investigating the impact of the anticorisin monoclonal antibody in a general model of acute lung injury, we further unravel the potential of corisin to impact such diseases. These results underscore the role of corisin in the pathogenesis of acute exacerbation of pulmonary fibrosis and acute lung injury and provide a novel approach to treating this incurable disease.

摘要

特发性肺纤维化是一种病因不明的不可治愈的疾病。特发性肺纤维化急性加重与高死亡率相关。肺上皮细胞的过度凋亡发生在肺纤维化急性加重中。我们最近发现了 corisin，一种触发肺纤维化急性加重的促凋亡肽。在这里，我们提供了对 corisin 加工和释放机制的深入了解。此外，我们证明了一种抗 corisin 单克隆抗体通过显著抑制人转化生长因子β1 模型中的急性加重和博来霉素模型中的急性肺损伤，从而改善肺纤维化。通过研究抗 corisin 单克隆抗体在一般急性肺损伤模型中的影响，我们进一步揭示了 corisin 影响此类疾病的潜力。这些结果强调了 corisin 在特发性肺纤维化和急性肺损伤急性加重发病机制中的作用，并为治疗这种不可治愈的疾病提供了一种新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/52ba7ec49efe/41467_2022_29064_Fig10_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/5253269d0bec/41467_2022_29064_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/bdec7245ea30/41467_2022_29064_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/52ba7ec49efe/41467_2022_29064_Fig10_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/216a077c6ad5/41467_2022_29064_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/ab54fd1d3def/41467_2022_29064_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/8e649bf26f21/41467_2022_29064_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/8ec230429edb/41467_2022_29064_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/513f83f63bb0/41467_2022_29064_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/5253269d0bec/41467_2022_29064_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/bdec7245ea30/41467_2022_29064_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd3a/8943153/52ba7ec49efe/41467_2022_29064_Fig10_HTML.jpg

相似文献

[1]
Inhibition of lung microbiota-derived proapoptotic peptides ameliorates acute exacerbation of pulmonary fibrosis.

Nat Commun. 2022-3-23

[2]
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[3]
A Staphylococcus pro-apoptotic peptide induces acute exacerbation of pulmonary fibrosis.

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[4]
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[5]
A Microbiome-Derived Peptide Induces Apoptosis of Cells from Different Tissues.

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[6]
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[7]
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[8]
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[9]
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[10]
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引用本文的文献

[1]
Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging.

Nat Commun. 2025-8-25

[2]
Exploratory Evaluation of Circulating Microbiota-Derived Corisin Levels in Women with Adverse Pregnancy Outcomes.

Antioxidants (Basel). 2025-5-31

[3]
Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.

Front Pharmacol. 2025-5-30

[4]
Sputum Microbiome, Potentially Pathogenic Organisms, and Clinical Outcomes in Japanese Patients with COPD and Moderate Airflow Limitation: The Prospective AERIS-J Study.

Int J Chron Obstruct Pulmon Dis. 2025-5-14

[5]
The lung microbiome in interstitial lung disease.

Breathe (Sheff). 2025-4-17

[6]
Inflammatory and Coagulation Marker Changes in PMX-DHP-Treated COVID-19 Patients.

Cureus. 2025-2-10

[7]
KAE ameliorates LPS-mediated acute lung injury by inhibiting PANoptosis through the intracellular DNA-cGAS-STING axis.

Front Pharmacol. 2025-1-7

[8]
Assessing the impact of gut microbiota and metabolic products on acute lung injury following intestinal ischemia-reperfusion injury: harmful or helpful?

Front Cell Infect Microbiol. 2024-12-2

[9]
Bleomycin-Induced Pulmonary Fibrosis in Transgenic Mice Carrying the Human rs35705950 Variant.

Cells. 2024-9-11

[10]
Pulmonary fibrosis: pathogenesis and therapeutic strategies.

MedComm (2020). 2024-9-23

本文引用的文献

[1]
A Microbiome-Derived Peptide Induces Apoptosis of Cells from Different Tissues.

Cells. 2021-10-26

[2]
Emerging connectivity of programmed cell death pathways and its physiological implications.

Nat Rev Mol Cell Biol. 2020-9-1

[3]
Serum mitochondrial DNA predicts the risk of acute exacerbation and progression of idiopathic pulmonary fibrosis.

Eur Respir J. 2021-1-21

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Eur Respir Rev. 2020-7-21

[5]
Pulmonary fibrosis and COVID-19: the potential role for antifibrotic therapy.

Lancet Respir Med. 2020-5-15

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Synthetic biology principles for the design of protein with novel structures and functions.

FEBS Lett. 2020-7

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Mitochondria dysfunction and metabolic reprogramming as drivers of idiopathic pulmonary fibrosis.

Redox Biol. 2020-6

[8]
A Staphylococcus pro-apoptotic peptide induces acute exacerbation of pulmonary fibrosis.

Nat Commun. 2020-3-24

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[Research advances in the mechanism of pulmonary fibrosis induced by coronavirus disease 2019 and the corresponding therapeutic measures].

Zhonghua Shao Shang Za Zhi. 2020-8-20

[10]
Molecular Dynamics of Lipopolysaccharide-Induced Lung Injury in Rodents.

Front Physiol. 2020-2-5

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