Journal of respiratory biology and translational medicine最新文献

Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases. 聚焦化与肺部疾病衰老之间的新机制联系

Journal of respiratory biology and translational medicine Pub Date : 2026-01-01 Epub Date: 2026-06-23 DOI: 10.70322/jrbtm.2026.10005

Snehalakshmi Kavacheri Subramaniam, Minxuan Hu, Wenjing Gu, Angle Xu, Peisong Gao

{"title":"Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.","authors":"Snehalakshmi Kavacheri Subramaniam, Minxuan Hu, Wenjing Gu, Angle Xu, Peisong Gao","doi":"10.70322/jrbtm.2026.10005","DOIUrl":"10.70322/jrbtm.2026.10005","url":null,"abstract":"Cellular senescence is increasingly recognized as a key driver of chronic lung diseases, contributing to persistent inflammation, impaired tissue repair, and pathological remodeling. In parallel, aberrant protein fucosylation has emerged as an important regulator of epithelial function and immune signaling in the respiratory tract. Recent evidence suggests that these processes may be mechanistically linked rather than independently dysregulated. In particular, core fucosylation mediated by fucosyltransferases, such as fucosyltransferases 8 (FUT8), can modulate receptor activity and amplify signaling pathways, including TGF-β/Smad and PI3K/Akt, that are central to the induction and maintenance of cellular senescence. These interactions may promote epithelial dysfunction, the senescence-associated secretory phenotype (SASP) production, and pro-fibrotic remodeling in diseases such as COPD, asthma, and idiopathic pulmonary fibrosis. In this review, we synthesize current knowledge on cellular senescence and fucosylation in chronic lung disease and highlight emerging evidence linking these processes through shared signaling networks. We further discuss the potential of the fucosylation-senescence axis as a source of novel biomarkers and therapeutic targets. This review is among the first to integrate emerging evidence linking aberrant fucosylation with cellular senescence signaling in chronic lung diseases, thereby providing a conceptual framework for future mechanistic and translational studies.","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13384517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148611655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function. E3连接酶：尚待研究的肺免疫功能调节因子。

Journal of respiratory biology and translational medicine Pub Date : 2026-01-01 Epub Date: 2026-08-12 DOI: 10.70322/jrbtm.2026.10006

Samuel Speaks, Anthony Pastore, MuChun Tsai

{"title":"MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.","authors":"Samuel Speaks, Anthony Pastore, MuChun Tsai","doi":"10.70322/jrbtm.2026.10006","DOIUrl":"10.70322/jrbtm.2026.10006","url":null,"abstract":"Membrane-associated RING-CH (MARCH) ligases are a family of 11 ubiquitin E3 ligases that regulate protein stability, trafficking, and signaling across diverse cellular contexts. Although MARCH ligases have been studied most extensively in immune regulation, antigen presentation, viral restriction, and cellular homeostasis, their roles in pulmonary biology remain incompletely defined. The lung is a highly specialized environmental interface that must preserve gas exchange while continuously responding to infectious, inflammatory, and sterile insults. These demands require careful regulation of epithelial and endothelial barrier integrity, innate and adaptive immune activation, and tissue repair. Current work suggests that MARCH ligases influence many of these processes by regulating inflammatory responses, cytokine receptors, antiviral signaling mediators, viral proteins, mitochondrial fission or fusion, junctional molecules, ciliary components, and remodeling pathways. In this review, we summarize current knowledge and highlight gaps in the understanding of MARCH ligase expression and function in lung-relevant cell types and disease contexts. Defining how MARCH ligases operate within specific lung compartments may reveal new regulatory mechanisms governing pulmonary immunity, barrier function, host defense, and lung remodeling.","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"3 3","pages":"10006"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13600764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149043277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Novel Therapeutic Targets of Endothelial Inflammation in Acute Lung Injury and Acute Respiratory Distress Syndrome. 内皮炎症在急性肺损伤和急性呼吸窘迫综合征中的新治疗靶点。

Journal of respiratory biology and translational medicine Pub Date : 2026-01-01 Epub Date: 2026-02-06 DOI: 10.70322/jrbtm.2026.10001

Yunchao Su

引用次数: 0

Harnessing Artificial Intelligence for Hypothesis Generation in Childhood Asthma: Insights from NHANES. 利用人工智能对儿童哮喘的假设生成：来自NHANES的见解。

Journal of respiratory biology and translational medicine Pub Date : 2026-01-01 Epub Date: 2026-04-28 DOI: 10.70322/jrbtm.2026.10003

Jing Liu, Yueh-Ying Han, Xiangyu Ye, Franziska J Rosser, Kristina M Gaietto, Chongyue Zhao, Wei Chen, Juan C Celedón

{"title":"Harnessing Artificial Intelligence for Hypothesis Generation in Childhood Asthma: Insights from NHANES.","authors":"Jing Liu, Yueh-Ying Han, Xiangyu Ye, Franziska J Rosser, Kristina M Gaietto, Chongyue Zhao, Wei Chen, Juan C Celedón","doi":"10.70322/jrbtm.2026.10003","DOIUrl":"10.70322/jrbtm.2026.10003","url":null,"abstract":"Although large language models (LLMs) have undergone substantial development, their applicability to epidemiological research has not been sufficiently examined. This study aims to develop and evaluate an LLM-based framework for hypothesis generation and testing, demonstrating its application in childhood asthma in the National Health and Nutrition Examination Survey (NHANES). Pilot study was conducted to explore factors associated with childhood asthma in the 2001-2020 NHANES cycles. A modular agent system was developed, including Database Query, Statistic, Paper Search, and Paper Download tools, along with two LLM models (Key Generator and Hypothesis Tester). Multivariable logistic regression was used to test for the association between each variable and current asthma, generating a tentative affirmative claim. The Key Generator module produced keywords for literature search, the Paper Search and Paper Download tools queried PubMed and retrieved relevant studies, and the Hypothesis Tester module synthesized evidence and determined the support for claims for each variable. Keywords and conclusions were reviewed by researchers and validated using multiple LLMs (ChatGPT, DeepSeek, and Gemini) to ensure consistency and robustness. 25,839 children with (n = 2928) and without (n = 22,911) current asthma, and 10,359 variables were included in the multivariable analysis, which yielded 100 variables associated with asthma. Of these, 21 were directly related to asthma (supporting published studies), 43 were indirectly related to asthma (based on background knowledge, though not explicitly discussed in the available publications), and 34 were unrelated to asthma. Two variables were excluded due to a lack of discriminative keywords. This study demonstrates the effectiveness of LLM-based models for generating and testing hypotheses about childhood asthma.","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"3 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13278482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148297942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic Strategies for Labeling AT2 Cells in Murine Lung via Abca3 and Etv5-Driven Reporters. 利用Abca3和etv5驱动报告基因标记小鼠肺AT2细胞的遗传策略

Journal of respiratory biology and translational medicine Pub Date : 2026-01-01 Epub Date: 2026-02-06 DOI: 10.70322/jrbtm.2026.10002

Xue Liu, Xuexi Zhang, Zekun Li, Vrishika Kulur, Ningshan Liu, Jiurong Liang, Dianhua Jiang

引用次数: 0

Striking Surge in Lung Cancer Incidence in Children of Early Life. 早期儿童肺癌发病率显著上升。

Journal of respiratory biology and translational medicine Pub Date : 2026-01-01 Epub Date: 2026-05-28 DOI: 10.70322/jrbtm.2026.10004

Nobel Chenggong Zong, Jessica Johal, Heather Liu, Hua Cai

{"title":"Striking Surge in Lung Cancer Incidence in Children of Early Life.","authors":"Nobel Chenggong Zong, Jessica Johal, Heather Liu, Hua Cai","doi":"10.70322/jrbtm.2026.10004","DOIUrl":"10.70322/jrbtm.2026.10004","url":null,"abstract":"Lung cancer ranks first in mortality and the third in total cancer cases diagnosed in the US. The epidemiological trends may vary among different age groups, while the dynamics of risk factors evolve as well. We aim to carefully characterize trends of lung cancer among different age groups in the past two decades, by accessing the Surveillance, Epidemiology, and End Results (SEER) datasets from the National Cancer Institute (NCI), and to delineate possible root causes. The SEER datasets were obtained from NCI. Data on environmental risk factors were acquired from the Environmental Protection Agency and the United States Geological Survey. The tobacco consumption data were sourced from the Centers for Disease Control and Prevention. Trends were examined statistically with the Mann-Kendall algorithm. The incidence rate of lung cancer in the <15 age group has been rising in the past two decades, most strikingly among infants in the 0 age group (at birth to less than 1 year old). These findings were unique for lung cancer. The usage of e-Cigarettes among pregnant women increased, while the potential influence of other known risk factors was on the decline. A shrinkage of the infant population and a higher rate of pregnancy loss were observed during the same timespan. A striking rise in lung cancer incidence among infants has been identified that is opposite to the declining trend in the overall population, which might be related to increased e-Cigarette use in pregnant women. Urgent further investigation is warranted to safeguard the newborn population from being continuously affected potentially by lung cancer.","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"3 2","pages":"10004"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149043183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis. 肺纤维化中肌成纤维细胞转化的机制和治疗潜力

Journal of respiratory biology and translational medicine Pub Date : 2025-03-01 Epub Date: 2025-03-07 DOI: 10.70322/jrbtm.2025.10001

Tianming Zhao, Yunchao Su

{"title":"Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.","authors":"Tianming Zhao, Yunchao Su","doi":"10.70322/jrbtm.2025.10001","DOIUrl":"10.70322/jrbtm.2025.10001","url":null,"abstract":"Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, and fatal disease with an increasing incidence and limited therapeutic options. It is characterized by the formation and deposition of excess extracellular matrix proteins resulting in the gradual replacement of normal lung architecture by fibrous tissue. The cellular and molecular mechanism of IPF has not been fully understood. A hallmark in IPF is pulmonary fibroblast to myofibroblast transformation (FMT). During excessive lung repair upon exposure to harmful stimuli, lung fibroblasts transform into myofibroblasts under stimulation of cytokines, chemokines, and vesicles from various cells. These mediators interact with lung fibroblasts, initiating multiple signaling cascades, such as TGFβ1, MAPK, Wnt/β-catenin, NF-κB, AMPK, endoplasmic reticulum stress, and autophagy, contributing to lung FMT. Furthermore, single-cell transcriptomic analysis has revealed significant heterogeneity among lung myofibroblasts, which arise from various cell types and are adapted to the altered microenvironment during pathological lung repair. This review provides an overview of recent research on the origins of lung myofibroblasts and the molecular pathways driving their formation, with a focus on the interactions between lung fibroblasts and epithelial cells, endothelial cells, and macrophages in the context of lung fibrosis. Based on these molecular insights, targeting the lung FMT could offer promising avenues for the treatment of IPF.","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

State of the ART: Drug Screening Reveals Artesunate as a Promising Anti-Fibrosis Therapy. ART的现状：药物筛选显示青蒿琥酯是一种很有前途的抗纤维化疗法。

Journal of respiratory biology and translational medicine Pub Date : 2025-03-01 Epub Date: 2024-12-16 DOI: 10.70322/jrbtm.2024.10023

Yujie Qiao, Jiurong Liang, Dianhua Jiang

引用次数: 0

The Multifaceted Roles of Neutrophil Death in COPD and Lung Cancer. 中性粒细胞死亡在慢性阻塞性肺病和肺癌中的多重作用。

Journal of respiratory biology and translational medicine Pub Date : 2025-03-01 Epub Date: 2024-12-09 DOI: 10.70322/jrbtm.2024.10022

Arabella Wan, Dongshi Chen

{"title":"The Multifaceted Roles of Neutrophil Death in COPD and Lung Cancer.","authors":"Arabella Wan, Dongshi Chen","doi":"10.70322/jrbtm.2024.10022","DOIUrl":"10.70322/jrbtm.2024.10022","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) and lung cancer are closely linked, with individuals suffering from COPD at a significantly higher risk of developing lung cancer. The mechanisms driving this increased risk are multifaceted, involving genomic instability, immune dysregulation, and alterations in the lung environment. Neutrophils, the most abundant myeloid cells in human blood, have emerged as critical regulators of inflammation in both COPD and lung cancer. Despite their short lifespan, neutrophils contribute to disease progression through various forms of programmed cell death, including apoptosis, necroptosis, ferroptosis, pyroptosis, and NETosis, a form of neutrophil death with neutrophil extracellular traps (NETs) formation. These distinct death pathways affect inflammatory responses, tissue remodeling, and disease progression in COPD and lung cancer. This review provides an in-depth exploration of the mechanisms regulating neutrophil death, the interplay between various cell death pathways, and their influence on disease progression. Additionally, we highlight emerging therapeutic approaches aimed at targeting neutrophil death pathways, presenting promising new interventions to enhance treatment outcomes in COPD and lung cancer.","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

USP11 Promotes Endothelial Apoptosis-Resistance in Pulmonary Arterial Hypertension by Deubiquitinating HINT3. USP11通过去泛素化HINT3促进肺动脉高压内皮细胞凋亡抵抗。

Journal of respiratory biology and translational medicine Pub Date : 2025-03-01 Epub Date: 2025-03-24 DOI: 10.70322/jrbtm.2025.10002

Bum-Yong Kang, Jiwoong Choi, Victor Tseng, Yutong Zhao, Jing Zhao, Robert S Stearman, Wilbur A Lam, Viranuj Sueblinvong, Benjamin T Kopp, Michael J Passineau, Changwon Park, John Lister, Raymond J Benza, Andrew J Jang

{"title":"USP11 Promotes Endothelial Apoptosis-Resistance in Pulmonary Arterial Hypertension by Deubiquitinating HINT3.","authors":"Bum-Yong Kang, Jiwoong Choi, Victor Tseng, Yutong Zhao, Jing Zhao, Robert S Stearman, Wilbur A Lam, Viranuj Sueblinvong, Benjamin T Kopp, Michael J Passineau, Changwon Park, John Lister, Raymond J Benza, Andrew J Jang","doi":"10.70322/jrbtm.2025.10002","DOIUrl":"10.70322/jrbtm.2025.10002","url":null,"abstract":"Pulmonary arterial hypertension (PAH) is a progressive, lethal, and incurable disease of the pulmonary vasculature. A previous genome-wide association study (GWAS) with Affymetrix microarray analysis data exhibited elevated histidine triad nucleotide-binding protein 3 (HINT3) in the lung samples of PAH compared to control subjects (failed donors, FD) and the positive correlations of HINT3 with deubiquitinase USP11 and B-cell lymphoma 2 (BCL2). In this study, we aim to investigate the roles and interplay of USP11 and HINT3 in the apoptosis resistance of PAH. The levels of USP11 and HINT3 were increased in the lungs of idiopathic PAH (IPAH) patients and Hypoxia/Sugen-treated mice. USP11 and HINT3 interacted physically, as shown by co-immunoprecipitation (co-IP) assay in human pulmonary arterial endothelial cells (HPAECs). HINT3 was degraded by polyubiquitination, which was reversed by USP11. Furthermore, HINT3 interacted with the anti-apoptotic mediator, BCL2. Overexpression of USP11 increased BCL2 content, congruent to elevated lung tissue levels seen in IPAH patients and Hypoxia/Sugen-treated mice. Conversely, the knockdown of HINT3 function led to a depletion of BCL2. Thus, we conclude that USP11 stabilizes HINT3 activation, which contributes to endothelial apoptosis-resistance of pulmonary arterial endothelial cells in PAH. This can potentially be a novel therapeutic target for ubiquitination modulators for PAH.","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12080269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0