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Article ; Online: Unveiling the Intricacies of Autophagy in Asthma: Unraveling Novel Therapeutic Avenues.

Peng, Junjun / Lu, Na / Hua, Shucheng / Song, Lei / Liu, Han

Frontiers in bioscience (Landmark edition)

2024 Volume 29, Issue 1, Page(s) 22

Abstract: Understanding the pathogenesis of different phenotypes of asthma, including glucocorticoid-dependent and glucocorticoid-resistant asthma, is crucial for the development of effective treatments. Autophagy, a fundamental cellular process involved in cell ... ...

Abstract	Understanding the pathogenesis of different phenotypes of asthma, including glucocorticoid-dependent and glucocorticoid-resistant asthma, is crucial for the development of effective treatments. Autophagy, a fundamental cellular process involved in cell homeostasis, has been implicated in asthma, although the exact mechanisms remain unclear. Recent studies have identified autophagy activation in eosinophilic, neutrophilic, and paucigranulocytic asthma, providing novel insights into the disease. This comprehensive review examines the role of autophagy in the pathogenesis and treatment of asthma, with a focus on various cell types. The goal is to uncover potential therapeutic targets and innovative treatment modalities to improve patient outcomes in clinical settings.
MeSH term(s)	Humans ; Neutrophils/metabolism ; Glucocorticoids/therapeutic use ; Asthma/drug therapy ; Asthma/metabolism ; Autophagy ; Phenotype ; Inflammation/metabolism
Chemical Substances	Glucocorticoids
Language	English
Publishing date	2024-02-10
Publishing country	Singapore
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2704569-9
ISSN	2768-6698 ; 2768-6698
ISSN (online)	2768-6698
ISSN	2768-6698
DOI	10.31083/j.fbl2901022
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Article ; Online: The versatile defender: exploring the multifaceted role of p62 in intracellular bacterial infection.

Zhou, Yuhao / Hua, Shucheng / Song, Lei

Frontiers in cellular and infection microbiology

2023 Volume 13, Page(s) 1180708

Abstract: As a highly conserved, multifunctional protein with multiple domains, p62/SQSTM1 plays a crucial role in several essential cellular activities, particularly selective autophagy. Recent research has shown that p62 is crucial in eradicating intracellular ... ...

Abstract	As a highly conserved, multifunctional protein with multiple domains, p62/SQSTM1 plays a crucial role in several essential cellular activities, particularly selective autophagy. Recent research has shown that p62 is crucial in eradicating intracellular bacteria by xenophagy, a selective autophagic process that identifies and eliminates such microorganisms. This review highlights the various roles of p62 in intracellular bacterial infections, including both direct and indirect, antibacterial and infection-promoting aspects, and xenophagy-dependent and independent functions, as documented in published literature. Additionally, the potential applications of synthetic drugs targeting the p62-mediated xenophagy mechanism and unresolved questions about p62's roles in bacterial infections are also discussed.
MeSH term(s)	Humans ; Autophagy ; Bacterial Infections ; Sequestosome-1 Protein/metabolism
Chemical Substances	Sequestosome-1 Protein ; SQSTM1 protein, human
Language	English
Publishing date	2023-05-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2023.1180708
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Article: Ferroptosis in pulmonary fibrosis: an emerging therapeutic target.

Wang, Chunyan / Hua, Shucheng / Song, Lei

Frontiers in physiology

2023 Volume 14, Page(s) 1205771

Abstract: In recent years, the role of ferroptosis in pulmonary fibrosis has garnered increasing interest as a potential therapeutic target. Pulmonary fibrosis is a pathological process characterized by the accumulation of extracellular matrix in affected lung ... ...

Abstract	In recent years, the role of ferroptosis in pulmonary fibrosis has garnered increasing interest as a potential therapeutic target. Pulmonary fibrosis is a pathological process characterized by the accumulation of extracellular matrix in affected lung tissues, and currently, there are no effective therapies for preventing or reversing the fibrotic lesions. Ferroptosis is a form of programmed cell death that is regulated by a network of enzymes and signaling pathways. Dysregulation of ferroptosis has been implicated in several diseases, including pulmonary fibrosis. The accumulation of lipid peroxides in the course of ferroptosis causes damage to cell membranes and other cellular components, leading ultimately to cell death. Relevant targets for therapeutic intervention in ferroptosis include key enzymes, such as glutathione peroxidase 4, transcription factors like nuclear factor erythroid 2-related factor 2, and iron chelation. This review provides an overview of the emerging role of ferroptosis in pulmonary fibrosis and highlights potential therapeutic targets in this pathway. Further research is needed to develop safe and effective approaches targeting ferroptosis in treatment of pulmonary fibrosis.
Language	English
Publishing date	2023-08-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1205771
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Article ; Online: ncRNAs-mediated TIMELESS overexpression in lung adenocarcinoma correlates with reduced tumor immune cell infiltration and poor prognosis.

Gao, Xinliang / Tang, Mingbo / Tian, Suyan / Li, Jialin / Wei, Shixiong / Hua, Shucheng / Liu, Wei

PloS one

2024 Volume 19, Issue 1, Page(s) e0296829

Abstract: Lung adenocarcinoma (LUAD) has a poor prognosis. Circadian genes such as TIMELESS have been associated with several pathologies, including cancer. The expression of TIMELESS and the relationship between TIMELESS, infiltration of tumors and prognosis in ... ...

Abstract	Lung adenocarcinoma (LUAD) has a poor prognosis. Circadian genes such as TIMELESS have been associated with several pathologies, including cancer. The expression of TIMELESS and the relationship between TIMELESS, infiltration of tumors and prognosis in LUAD requires further investigation. In this study, we investigated the expression of TIMELESS and its association with survival across several types of human cancer using data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression Program. Noncoding RNAs (ncRNAs) regulating overexpression of TIMELESS in lung adenocarcinoma (LUAD) were explored with expression, correlation, and survival analyses. Immune cell infiltration and biomarkers were analyzed between different TIMELESS expression levels. The relationship between TIMELESS expression and immunophenoscores, which were used to predict response to immunotherapy, was evaluated. TIMELESS was identified as a potential oncogene in LUAD. NcRNA analysis showed MIR4435-2HG/hsa-miR-1-3p may interact with TIMELESS in a competitive endogenous RNA network in LUAD tumor tissues. Most immune cells were significantly decreased in TCGA LUAD tumor tissues with high TIMELESS expression except for CD4+T cells and Th2 cells. TIMELESS expression in LUAD tumor tissues was significantly negatively correlated with neutrophil biomarkers, dendritic cell biomarkers (HLA-DPB1, HLA-DQB1, HLA-DRA, HLA-DPA1, CD1C) and an immunophenoscore that predicted outcomes associated with the use of immune checkpoint inhibitors. These findings imply that ncRNAs-mediated TIMELESS overexpression in LUAD tumor tissues correlated with poor prognosis, reduced immune cell infiltration in the tumor microenvironment, and poor response to immune checkpoint inhibitors.
MeSH term(s)	Humans ; Adenocarcinoma of Lung ; Biomarkers ; Immune Checkpoint Inhibitors ; Lung Neoplasms ; Oncogenes ; RNA, Untranslated ; Tumor Microenvironment
Chemical Substances	Biomarkers ; Immune Checkpoint Inhibitors ; RNA, Untranslated ; TIMELESS protein, human
Language	English
Publishing date	2024-01-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0296829
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Article ; Online: Trim27 aggravates airway inflammation and oxidative stress in asthmatic mice via potentiating the NLRP3 inflammasome.

Liu, Kaimeng / Gu, Yue / Gu, Sanwei / Song, Lei / Hua, Shucheng / Li, Dan / Tang, Mingbo

International immunopharmacology

2024 Volume 134, Page(s) 112199

Abstract: Asthma is a prevalent chronic respiratory disease, yet understanding its ecology and pathogenesis remains a challenge. Trim27, a ubiquitination ligase belonging to the TRIM (tripartite motif-containing) family, has been implicated in regulating multiple ... ...

Abstract	Asthma is a prevalent chronic respiratory disease, yet understanding its ecology and pathogenesis remains a challenge. Trim27, a ubiquitination ligase belonging to the TRIM (tripartite motif-containing) family, has been implicated in regulating multiple pathophysiological processes such as inflammation, oxidative stress, apoptosis, and cell proliferation. However, the role of Trim27 in asthma has not been investigated. Our study found that Trim27 expression significantly increases in the airway epithelium of asthmatic mice. Knockdown of Trim27 expression effectively relieved ovalbumin (OVA)-induced airway hyperresponsiveness (AHR) and lung tissue histopathological changes. Moreover, Trim27 knockdown exhibited a significant reduction in airway inflammation and oxidative stress in asthmatic mice, and in vitro analysis confirmed the favorable effect of Trim27 deletion on inflammation and oxidative stress in mouse airway epithelial cells. Furthermore, our study revealed that deletion of Trim27 in MLE12 cells significantly decreased NLRP3 inflammasome activation, as evidenced by reduced expression of NLRP3, ASC, and pro-IL-1β mRNA. This downregulation was reversed when Trim27, but not its mutant lacking ubiquitination ligase activity, was replenished in these cells. Consistent with these findings, protein levels of NLRP3, pro-caspase-1, pro-IL-1β, cleaved-caspase-1, and cleaved-IL-1β were higher in Trim27-replenished cells compared to cells expressing Trim27C/A. Functionally, the downregulation of IL-1β and IL-18 levels induced by Trim27 deletion was rescued by replenishing Trim27. Overall, our findings provide evidence that Trim27 contributes to airway inflammation and oxidative stress in asthmatic mice via NLRP3 inflammasome activation, providing crucial insights into potential therapeutic interventions targeting Trim27 as a way to treat asthma.
Language	English
Publishing date	2024-05-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2024.112199
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Article ; Online: The Correlation of PM2.5 Exposure with Acute Attack and Steroid Sensitivity in Asthma.

Luo, Jingjing / Liu, Han / Hua, Shucheng / Song, Lei

publication RETRACTED

BioMed research international

2022 Volume 2022, Page(s) 2756147

Abstract: Bronchial asthma is a common chronic inflammatory disease of the respiratory system. Asthma primarily manifests in reversible airflow limitation and airway inflammation, airway remodeling, and persistent airway hyperresponsiveness. PM2.5, also known as ... ...

Abstract	Bronchial asthma is a common chronic inflammatory disease of the respiratory system. Asthma primarily manifests in reversible airflow limitation and airway inflammation, airway remodeling, and persistent airway hyperresponsiveness. PM2.5, also known as fine particulate matter, is the main component of air pollution and refers to particulate matter with an aerodynamic diameter of ≤2.5
MeSH term(s)	Air Pollutants ; Air Pollution ; Asthma ; Humans ; Particulate Matter ; Steroids
Chemical Substances	Air Pollutants ; Particulate Matter ; Steroids
Language	English
Publishing date	2022-08-18
Publishing country	United States
Document type	Journal Article ; Review ; Retracted Publication
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2022/2756147
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Article ; Online: PM2.5 Exposure and Asthma Development: The Key Role of Oxidative Stress.

Liu, Kaimeng / Hua, Shucheng / Song, Lei

Oxidative medicine and cellular longevity

2022 Volume 2022, Page(s) 3618806

Abstract: Oxidative stress is defined as the imbalance between reactive oxygen species (ROS) production and the endogenous antioxidant defense system, leading to cellular damage. Asthma is a common chronic inflammatory airway disease. The presence of asthma tends ... ...

Abstract	Oxidative stress is defined as the imbalance between reactive oxygen species (ROS) production and the endogenous antioxidant defense system, leading to cellular damage. Asthma is a common chronic inflammatory airway disease. The presence of asthma tends to increase the production of reactive oxygen species (ROS), and the antioxidant system in the lungs is insufficient to mitigate it. Therefore, asthma can lead to an exacerbation of airway hyperresponsiveness and airway inflammation. PM2.5 exposure increases ROS levels. Meanwhile, the accumulation of ROS will further enhance the oxidative stress response, resulting in DNA, protein, lipid, and other cellular and molecular damage, leading to respiratory diseases. An in-depth study on the relationship between oxidative stress and PM2.5-related asthma is helpful to understand the pathogenesis and progression of the disease and provides a new direction for the treatment of the disease. This paper reviews the research progress of oxidative stress in PM2.5-induced asthma as well as highlights the therapeutic potentials of antioxidant approaches in treatment of asthma.
MeSH term(s)	Antioxidants/metabolism ; Asthma/drug therapy ; Humans ; Oxidative Stress/physiology ; Particulate Matter/toxicity ; Pulmonary Disease, Chronic Obstructive ; Reactive Oxygen Species/metabolism
Chemical Substances	Antioxidants ; Particulate Matter ; Reactive Oxygen Species
Language	English
Publishing date	2022-04-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2022/3618806
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Article ; Online: TREX1 plays multiple roles in human diseases.

Wang, Qing / Du, Juan / Hua, Shucheng / Zhao, Ke

Cellular immunology

2022 Volume 375, Page(s) 104527

Abstract: Three-prime repair exonuclease 1 (TREX1) is a major 3'-5' DNA exonuclease, which digests cytosolic DNA to avoid inappropriate activation of the innate immune system. Besides the most studied exonuclease activity, the recently discovered functions of ... ...

Abstract	Three-prime repair exonuclease 1 (TREX1) is a major 3'-5' DNA exonuclease, which digests cytosolic DNA to avoid inappropriate activation of the innate immune system. Besides the most studied exonuclease activity, the recently discovered functions of TREX1, such as regulating the oligosaccharyltransferase complex and triggering proteasome-mediated degradation, are also indispensable to prevent innate immune activation. However, mounting evidence indicates a dual role of TREX1 in human diseases. In cancer and radiotherapy, the digestion of immunogenic DNA by TREX1 inhibits antitumor immunity. Moreover, TREX1 also processes specific chromosomal abnormalities upon nuclear membrane rupture, which induces DNA damage. In this review, we summarize previous studies assessing the function and mechanisms of TREX1 in autoimmune diseases, inflammatory diseases, and cancer and discuss the relationship between the function and its associated diseases. By analyzing the various roles of TREX1 under different conditions, we explored the remaining questions regarding the molecular mechanism of TREX1.
MeSH term(s)	Autoimmune Diseases/genetics ; Cell Nucleus ; DNA ; Exodeoxyribonucleases/genetics ; Exodeoxyribonucleases/metabolism ; Humans ; Phosphoproteins/genetics ; Phosphoproteins/metabolism
Chemical Substances	Phosphoproteins ; DNA (9007-49-2) ; Exodeoxyribonucleases (EC 3.1.-) ; three prime repair exonuclease 1 (EC 3.1.16.-)
Language	English
Publishing date	2022-04-21
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80094-6
ISSN	1090-2163 ; 0008-8749
ISSN (online)	1090-2163
ISSN	0008-8749
DOI	10.1016/j.cellimm.2022.104527
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Article ; Online: Perspectives and controversies regarding the use of natural products for the treatment of lung cancer.

Wen, Tingting / Song, Lei / Hua, Shucheng

Cancer medicine

2021 Volume 10, Issue 7, Page(s) 2396–2422

Abstract: Lung cancer is the leading cause of cancer-related mortality both in men and women and accounts for 18.4% of all cancer-related deaths. Although advanced therapy methods have been developed, the prognosis of lung cancer patients remains extremely poor. ... ...

Abstract	Lung cancer is the leading cause of cancer-related mortality both in men and women and accounts for 18.4% of all cancer-related deaths. Although advanced therapy methods have been developed, the prognosis of lung cancer patients remains extremely poor. Over the past few decades, clinicians and researchers have found that chemical compounds extracted from natural products may be useful for treating lung cancer. Drug formulations derived from natural compounds, such as paclitaxel, doxorubicin, and camptothecin, have been successfully used as chemotherapeutics for lung cancer. In recent years, hundreds of new natural compounds that can be used to treat lung cancer have been found through basic and sub-clinical research. However, there has not been a corresponding increase in the number of drugs that have been used in a clinical setting. The probable reasons may include low solubility, limited absorption, unfavorable metabolism, and severe side effects. In this review, we present a summary of the natural compounds that have been proven to be effective for the treatment of lung cancer, as well as an understanding of the mechanisms underlying their pharmacological effects. We have also highlighted current controversies and have attempted to provide solutions for the clinical translation of these compounds.
MeSH term(s)	Antineoplastic Agents, Phytogenic/therapeutic use ; Biological Products/therapeutic use ; Clinical Trials as Topic ; Drug Discovery/methods ; Drug Evaluation, Preclinical/methods ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology
Chemical Substances	Antineoplastic Agents, Phytogenic ; Biological Products
Language	English
Publishing date	2021-03-02
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2045-7634
ISSN (online)	2045-7634
DOI	10.1002/cam4.3660
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Article ; Online: Proteomic and ultrastructural analysis of Clara cell and type II alveolar epithelial cell-type lung cancer cells.

Hou, Wen-Li / Chang, Ming / Liu, Xiao-Feng / Hu, Lin-Sen / Hua, Shu-Cheng

Translational cancer research

2022 Volume 9, Issue 2, Page(s) 565–576

Abstract: Background: Currently, the identification of Clara cell and type II alveolar epithelial cell-type cancer cells requires electron microscopy, which is a time-consuming and expensive process involving a complicated tissue sampling procedure. The aim of ... ...

Abstract	Background: Currently, the identification of Clara cell and type II alveolar epithelial cell-type cancer cells requires electron microscopy, which is a time-consuming and expensive process involving a complicated tissue sampling procedure. The aim of this study was to identify unique biomarkers for Clara cell and type II alveolar epithelial cell-type lung cancer cells, respectively, with proteomic profiling. Methods: Six human lung adenocarcinoma cell lines (A549, NCI-H358, NCI-H1650, HCC827, NCI-H1395, and NCI-H1975) were investigated for their ultrastructural characteristics. The differentially expressed proteins (DEPs) were screened between NCI-H358 cells (Clara cell type) and A549 cells (type II alveolar epithelial cell type) using two-dimensional difference gel electrophoresis (2D-DIGE) and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS/MS), and then they were validated by western blot. The protein expression levels of endoplasmic reticulum oxidoreductin 1-α (ERO1L), Clara cell 10-kD protein (CC10), and surfactant protein C (SP-C) were also determined in the six cell lines assayed. Results: NCI-H358 cells featured Clara cell differentiation; A549, NCI-H1975, and HCC827 cells had characteristics of type II alveolar epithelial cells; and NCI-H1395 and NCI-H1650 cells had no differentiation characteristics of any lung adenocarcinoma cell type. Five DEPs including ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1), cytokeratin 19 (CK19), cytokeratin 8 (CK8), ERO1L, and peroxiredoxin 2 (PRDX2) between NCI-H358 and A549 cells were identified for further validation; however, none of them showed suitability as an effective biomarker. Similarly, CC10 and SP-C were not appropriate biomarkers. Conclusions: Cytological subtypes of NCI-H1975 and HCC827 cells were identified, but no promising biomarker was discovered in the present study.
Language	English
Publishing date	2022-01-20
Publishing country	China
Document type	Journal Article
ZDB-ID	2901601-0
ISSN	2219-6803 ; 2218-676X
ISSN (online)	2219-6803
ISSN	2218-676X
DOI	10.21037/tcr.2019.12.04
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