Pub Date : 2024-12-01DOI: 10.1016/j.pccm.2024.08.009
Chunhui Yang , Wenwen Liu , Charles A. Powell , Qi Wang
Lung cancer is a leading cause of cancer-related mortality. The tumor microenvironment is a complex and heterogeneous cellular environment surrounding tumor cells, including cancer-associated fibroblasts (CAFs), blood vessels, immune cells, the extracellular matrix, and various cytokines secreted by cells. CAFs are highly heterogeneous and play crucial roles in lung cancer. This review highlights recent advances in the understanding of CAFs in lung cancer, focusing on their heterogeneity and functions in tumorigenesis, progression, angiogenesis, invasion, metastasis, therapy resistance, tumor immune suppression, and targeted therapy responses. Additionally, we explore the underlying mechanisms and the potential of CAFs as a target in the development of innovative therapies for lung cancer.
{"title":"Heterogeneity and therapeutic implications of cancer-associated fibroblasts in lung cancer: Recent advances and future perspectives","authors":"Chunhui Yang , Wenwen Liu , Charles A. Powell , Qi Wang","doi":"10.1016/j.pccm.2024.08.009","DOIUrl":"10.1016/j.pccm.2024.08.009","url":null,"abstract":"<div><div>Lung cancer is a leading cause of cancer-related mortality. The tumor microenvironment is a complex and heterogeneous cellular environment surrounding tumor cells, including cancer-associated fibroblasts (CAFs), blood vessels, immune cells, the extracellular matrix, and various cytokines secreted by cells. CAFs are highly heterogeneous and play crucial roles in lung cancer. This review highlights recent advances in the understanding of CAFs in lung cancer, focusing on their heterogeneity and functions in tumorigenesis, progression, angiogenesis, invasion, metastasis, therapy resistance, tumor immune suppression, and targeted therapy responses. Additionally, we explore the underlying mechanisms and the potential of CAFs as a target in the development of innovative therapies for lung cancer.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 4","pages":"Pages 240-249"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017303","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}
Pub Date : 2024-12-01DOI: 10.1016/j.pccm.2024.08.008
Xiaoyan Gai , Brian Allwood , Yongchang Sun
Tuberculosis (TB) significantly increases the risk of developing chronic obstructive pulmonary disease (COPD), positioning TB-associated COPD (TB-COPD) as a distinct category within the spectrum of respiratory diseases prevalent, especially in low- and middle-income countries. This condition results from the body's immune response to TB, leading to prolonged inflammation and consequent persistent lung damage. Diagnostic approaches, particularly post-bronchodilator spirometry, are vital for identifying airflow obstruction and confirming TB-COPD. Furthermore, exploring potential biomarkers is crucial for a deeper insight into the pathogenesis of TB-COPD and the improvement of treatment strategies. Currently, this condition is primarily managed using inhaled bronchodilators, with cautious use of inhaled corticosteroids advised owing to the increased risk of developing TB. This review delves into the epidemiology, clinical manifestations, pulmonary function, and imaging characteristics of TB-COPD, scrutinizing current and prospective biomarkers and therapeutic strategies. Furthermore, it underscores the necessity for focused research to bridge the knowledge and treatment gaps in this complex condition.
{"title":"Advances in the awareness of tuberculosis-associated chronic obstructive pulmonary disease","authors":"Xiaoyan Gai , Brian Allwood , Yongchang Sun","doi":"10.1016/j.pccm.2024.08.008","DOIUrl":"10.1016/j.pccm.2024.08.008","url":null,"abstract":"<div><div>Tuberculosis (TB) significantly increases the risk of developing chronic obstructive pulmonary disease (COPD), positioning TB-associated COPD (TB-COPD) as a distinct category within the spectrum of respiratory diseases prevalent, especially in low- and middle-income countries. This condition results from the body's immune response to TB, leading to prolonged inflammation and consequent persistent lung damage. Diagnostic approaches, particularly post-bronchodilator spirometry, are vital for identifying airflow obstruction and confirming TB-COPD. Furthermore, exploring potential biomarkers is crucial for a deeper insight into the pathogenesis of TB-COPD and the improvement of treatment strategies. Currently, this condition is primarily managed using inhaled bronchodilators, with cautious use of inhaled corticosteroids advised owing to the increased risk of developing TB. This review delves into the epidemiology, clinical manifestations, pulmonary function, and imaging characteristics of TB-COPD, scrutinizing current and prospective biomarkers and therapeutic strategies. Furthermore, it underscores the necessity for focused research to bridge the knowledge and treatment gaps in this complex condition.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 4","pages":"Pages 250-256"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017226","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}
Pub Date : 2024-12-01DOI: 10.1016/j.pccm.2024.11.001
Jing Wu, Yingyao Chen, Mengqing Xie, Xin Yu, Chunxia Su
The innate immune system has a primary role in defending against external threats, encompassing viruses, bacteria, and fungi, thereby playing a pivotal role in establishing robust protection. Recent investigations have shed light on its importance in the progression of tumors, with a particular emphasis on lung cancer. Among the various signaling pathways implicated in this intricate process, the cGAS-STING pathway emerges as a significant participant. Cyclic GMP-AMP synthase (cGAS) discerns free DNA and activates the stimulator of interferon genes (STING), subsequently culminating in the secretion of cytokines and exerting inhibitory effects on tumor development. Consequently, researchers are increasingly interested in creating anticancer drugs that specifically target the cGAS-STING pathway, offering promising avenues for novel therapeutic interventions. The objective of this review is to present a comprehensive overview of the ongoing research on the cGAS-STING signaling pathway within the realm of lung cancer. The primary emphasis is on understanding its involvement in lung cancer development and assessing its viability as a target for innovative therapeutic options.
先天免疫系统在抵御包括病毒、细菌和真菌在内的外部威胁方面起着主要作用,因此在建立强大的保护方面起着关键作用。最近的研究揭示了它在肿瘤进展中的重要性,尤其是肺癌。在涉及这一复杂过程的各种信号通路中,cGAS-STING通路是一个重要的参与者。环GMP-AMP合成酶(Cyclic GMP-AMP synthase, cGAS)识别游离DNA,激活干扰素基因刺激因子(stimulator of interferon genes, STING),最终导致细胞因子的分泌,对肿瘤的发展起到抑制作用。因此,研究人员对开发针对cGAS-STING通路的抗癌药物越来越感兴趣,这为新的治疗干预提供了有希望的途径。本综述的目的是全面概述正在进行的肺癌领域的cGAS-STING信号通路的研究。主要重点是了解其在肺癌发展中的作用,并评估其作为创新治疗选择目标的可行性。
{"title":"cGAS-STING signaling pathway in lung cancer: Regulation on antitumor immunity and application in immunotherapy","authors":"Jing Wu, Yingyao Chen, Mengqing Xie, Xin Yu, Chunxia Su","doi":"10.1016/j.pccm.2024.11.001","DOIUrl":"10.1016/j.pccm.2024.11.001","url":null,"abstract":"<div><div>The innate immune system has a primary role in defending against external threats, encompassing viruses, bacteria, and fungi, thereby playing a pivotal role in establishing robust protection. Recent investigations have shed light on its importance in the progression of tumors, with a particular emphasis on lung cancer. Among the various signaling pathways implicated in this intricate process, the cGAS-STING pathway emerges as a significant participant. Cyclic GMP-AMP synthase (cGAS) discerns free DNA and activates the stimulator of interferon genes (STING), subsequently culminating in the secretion of cytokines and exerting inhibitory effects on tumor development. Consequently, researchers are increasingly interested in creating anticancer drugs that specifically target the cGAS-STING pathway, offering promising avenues for novel therapeutic interventions. The objective of this review is to present a comprehensive overview of the ongoing research on the cGAS-STING signaling pathway within the realm of lung cancer. The primary emphasis is on understanding its involvement in lung cancer development and assessing its viability as a target for innovative therapeutic options.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 4","pages":"Pages 257-264"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017231","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}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.05.002
Yin Zhu , Hui Shen , Andrew D Lerner , Qin Li , Si Chen , Lingxiao Zhou , Jiaqi Zhou , Yang Xia , Kopen Wang
Transbronchial needle aspiration (TBNA) is a commonly used sampling approach in the diagnosis of hilar and mediastinal lymphadenopathy as well as peripheral lesions. As a very important tool, the continued innovation of TBNA needles is a vital driving force for the development of the technique. Although TBNA plays an important role in interventional pulmonology, there are no clear standards guiding operators to choose an appropriate needle for their operation. In recent decades, with the advent of endobronchial ultrasound-guided TBNA (EBUS-TBNA), the real-time visualization of TBNA has been enabled. These modern TBNA needles, such as ViziShot2, FLEX 19G, Acquire FNB, and EchoTip ProCore, have made significant progress in specimen collection, convenience, and safety, though still remain grounded in the basic premise and initial upgrades to the original conventional TBNA (cTBNA) needles. This review introduced the developmental history of WANG cTBNA needles, and summarized the lessons of success and failure and the enlightenments for currently used EBUS- and other emerging TBNA needles, aiming to provide a significant reference for pulmonologists who lived through the cTBNA era and for junior physicians who start working in the EBUS-TBNA era. Despite its long history, TBNA is still playing significant roles in the diagnosis of pulmonary diseases. A deeper understanding from the historical perspectives would facilitate continued innovations in the field of TBNA and beyond.
{"title":"Evolution of transbronchial needle aspiration needles: Over the last half century","authors":"Yin Zhu , Hui Shen , Andrew D Lerner , Qin Li , Si Chen , Lingxiao Zhou , Jiaqi Zhou , Yang Xia , Kopen Wang","doi":"10.1016/j.pccm.2024.05.002","DOIUrl":"10.1016/j.pccm.2024.05.002","url":null,"abstract":"<div><div>Transbronchial needle aspiration (TBNA) is a commonly used sampling approach in the diagnosis of hilar and mediastinal lymphadenopathy as well as peripheral lesions. As a very important tool, the continued innovation of TBNA needles is a vital driving force for the development of the technique. Although TBNA plays an important role in interventional pulmonology, there are no clear standards guiding operators to choose an appropriate needle for their operation. In recent decades, with the advent of endobronchial ultrasound-guided TBNA (EBUS-TBNA), the real-time visualization of TBNA has been enabled. These modern TBNA needles, such as ViziShot2, FLEX 19G, Acquire FNB, and EchoTip ProCore, have made significant progress in specimen collection, convenience, and safety, though still remain grounded in the basic premise and initial upgrades to the original conventional TBNA (cTBNA) needles. This review introduced the developmental history of WANG cTBNA needles, and summarized the lessons of success and failure and the enlightenments for currently used EBUS- and other emerging TBNA needles, aiming to provide a significant reference for pulmonologists who lived through the cTBNA era and for junior physicians who start working in the EBUS-TBNA era. Despite its long history, TBNA is still playing significant roles in the diagnosis of pulmonary diseases. A deeper understanding from the historical perspectives would facilitate continued innovations in the field of TBNA and beyond.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 162-170"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324179","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}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.002
Jinsong Zhang , Natalie Vokes , Man Li , Jiachen Xu , Hua Bai , Jie Wang , Zhijie Wang , Jianjun Zhang
Targeted therapy has ushered in a new era of precision medicine for non-small cell lung cancer (NSCLC). Currently, epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) stand as the recommended first-line therapy for advanced NSCLC harboring sensitive EGFR mutations. Nevertheless, most patients inevitably confront the challenge of drug resistance. This phenomenon arises not solely from intrinsic alterations within cancer cells but also from the intricate dynamics of the tumor microenvironment and the complex interactions that occur between cancer cells and their immediate surroundings. This review consolidates the current knowledge regarding EGFR-TKI resistance mechanisms, with a specific emphasis on unraveling the role played by the tumor microenvironment. In addition, the review delineates strategic approaches to surmount TKI resistance, thereby enriching the understanding of the interplay between therapeutic agents and the intricate milieu surrounding cancer cells.
{"title":"Overcoming EGFR-TKI resistance by targeting the tumor microenvironment","authors":"Jinsong Zhang , Natalie Vokes , Man Li , Jiachen Xu , Hua Bai , Jie Wang , Zhijie Wang , Jianjun Zhang","doi":"10.1016/j.pccm.2024.08.002","DOIUrl":"10.1016/j.pccm.2024.08.002","url":null,"abstract":"<div><div>Targeted therapy has ushered in a new era of precision medicine for non-small cell lung cancer (NSCLC). Currently, epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) stand as the recommended first-line therapy for advanced NSCLC harboring sensitive <em>EGFR</em> mutations. Nevertheless, most patients inevitably confront the challenge of drug resistance. This phenomenon arises not solely from intrinsic alterations within cancer cells but also from the intricate dynamics of the tumor microenvironment and the complex interactions that occur between cancer cells and their immediate surroundings. This review consolidates the current knowledge regarding EGFR-TKI resistance mechanisms, with a specific emphasis on unraveling the role played by the tumor microenvironment. In addition, the review delineates strategic approaches to surmount TKI resistance, thereby enriching the understanding of the interplay between therapeutic agents and the intricate milieu surrounding cancer cells.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 151-161"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142323543","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}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.001
Han Yang , Si Chen , Jiayuan Sun , Felix J.F. Herth
Chronic inflammatory airway diseases, such as chronic bronchitis, chronic obstructive pulmonary disease, emphysema, and bronchial asthma, pose significant healthcare challenges. Interventional treatments offer promise as valuable complements to the optimal medical therapy recommended by the Global Initiative for Chronic Obstructive Lung Disease guideline and the Global Initiative for Asthma guideline. By directly accessing the airways, these minimally invasive procedures enable precise interventions. They encompass a wide range of techniques including bronchial thermoplasty and targeted lung denervation for both chronic obstructive pulmonary disease and severe asthma, bronchoscopic lung volume reduction (including the use of endobronchial valves, coils, and bronchoscopic thermal vapor ablation), airway bypass and peripheral stent placement for emphysema, bronchial rheoplasty and spray cryotherapy for chronic bronchitis, and other emerging methods. These interventional treatments aim to improve patients’ symptoms by reducing lung volume, alleviating hyperinflation, eliminating vagal innervation, disrupting hyperplastic goblet cells and thus reducing excessive mucus secretion, and weakening submucosal smooth muscles. This review highlights the potential advantages of interventional treatments for chronic inflammatory airway diseases and discusses relevant techniques tailored to specific disease subtypes. The overall aim is to assist interventional pulmonologists in selecting the most appropriate techniques for individual patients.
{"title":"Interventional pulmonology for chronic inflammatory airway diseases","authors":"Han Yang , Si Chen , Jiayuan Sun , Felix J.F. Herth","doi":"10.1016/j.pccm.2024.08.001","DOIUrl":"10.1016/j.pccm.2024.08.001","url":null,"abstract":"<div><div>Chronic inflammatory airway diseases, such as chronic bronchitis, chronic obstructive pulmonary disease, emphysema, and bronchial asthma, pose significant healthcare challenges. Interventional treatments offer promise as valuable complements to the optimal medical therapy recommended by the Global Initiative for Chronic Obstructive Lung Disease guideline and the Global Initiative for Asthma guideline. By directly accessing the airways, these minimally invasive procedures enable precise interventions. They encompass a wide range of techniques including bronchial thermoplasty and targeted lung denervation for both chronic obstructive pulmonary disease and severe asthma, bronchoscopic lung volume reduction (including the use of endobronchial valves, coils, and bronchoscopic thermal vapor ablation), airway bypass and peripheral stent placement for emphysema, bronchial rheoplasty and spray cryotherapy for chronic bronchitis, and other emerging methods. These interventional treatments aim to improve patients’ symptoms by reducing lung volume, alleviating hyperinflation, eliminating vagal innervation, disrupting hyperplastic goblet cells and thus reducing excessive mucus secretion, and weakening submucosal smooth muscles. This review highlights the potential advantages of interventional treatments for chronic inflammatory airway diseases and discusses relevant techniques tailored to specific disease subtypes. The overall aim is to assist interventional pulmonologists in selecting the most appropriate techniques for individual patients.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 171-181"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324180","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}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.004
Yang Zheng , Lei Lan , Gan Lu , Ya-dong Gao
Background
The urbanization and industrialization of East and Southeast Asia in decades past has significantly altered living environment and lifestyles, which may have complicated effects on the burden of asthma. We aim to examine the patterns and trends of asthma incidence rates in six major East and Southeast Asian countries as well as five major Western countries, and predict the numbers of new cases attributed to various factors.
Methods
Data on annual asthma incident cases and corresponding population by age group were drawn from 6 major selected East and Southeast Asian countries available in the Global Burden of Disease database, including China, Japan, Korea, Singapore, Philippines, and Thailand. We also collected data of five major high-income Western countries for comparative purposes. Two separate Bayesian age–period–cohort models, representing pre-COVID (model 1) and post-COVID (model 2) scenarios, were constructed to predict the asthma incidence until 2030.
Results
In model 1, the age-standardized incidence rate of asthma will be the highest in the US (1970.07 per 100,000, 95% confidence interval [CI] 533.05–4455.03), while the lowest incidence rate will be found in Singapore (296.72 per 100,000, 95% CI 135.16–899.55) in 2030. Between 1990 and 2030, the incidence of asthma is projected to increase in China and Thailand, with average annual percentages changes (AAPC) ranging from 0.70% to 1.80%. The remaining four Asian countries show a declining trend, with AAPC ranging from -0.51% to -2.00%. In model 2, the US is estimated to have the highest age-standardized incidence rate (902.71 per 100,000, 95% CI 375.44–2277.24), while Korea will have the lowest incidence rate (176.46 per 100,000, 95% CI 58.77–512.09) in 2030. A decrease in asthma incidence was observed in all countries with the overall AAPC ranging from -3.42% to -0.42%. Notably, a turning point was found around 2020, after which the incidence rates dropped significantly.
Conclusions
Pandemic-related factors may temporarily lower the incidence of asthma. The expected increasing asthma incidence in pre-COVID scenario (model 1) should still warrant attention from public health practitioners and call for efforts to reduce the burden of asthma.
{"title":"Patterns and trends in asthma incidence rates in main Asian and Western countries and their prediction to 2030","authors":"Yang Zheng , Lei Lan , Gan Lu , Ya-dong Gao","doi":"10.1016/j.pccm.2024.08.004","DOIUrl":"10.1016/j.pccm.2024.08.004","url":null,"abstract":"<div><h3>Background</h3><div>The urbanization and industrialization of East and Southeast Asia in decades past has significantly altered living environment and lifestyles, which may have complicated effects on the burden of asthma. We aim to examine the patterns and trends of asthma incidence rates in six major East and Southeast Asian countries as well as five major Western countries, and predict the numbers of new cases attributed to various factors.</div></div><div><h3>Methods</h3><div>Data on annual asthma incident cases and corresponding population by age group were drawn from 6 major selected East and Southeast Asian countries available in the Global Burden of Disease database, including China, Japan, Korea, Singapore, Philippines, and Thailand. We also collected data of five major high-income Western countries for comparative purposes. Two separate Bayesian age–period–cohort models, representing pre-COVID (model 1) and post-COVID (model 2) scenarios, were constructed to predict the asthma incidence until 2030.</div></div><div><h3>Results</h3><div>In model 1, the age-standardized incidence rate of asthma will be the highest in the US (1970.07 per 100,000, 95% confidence interval [CI] 533.05–4455.03), while the lowest incidence rate will be found in Singapore (296.72 per 100,000, 95% CI 135.16–899.55) in 2030. Between 1990 and 2030, the incidence of asthma is projected to increase in China and Thailand, with average annual percentages changes (AAPC) ranging from 0.70% to 1.80%. The remaining four Asian countries show a declining trend, with AAPC ranging from -0.51% to -2.00%. In model 2, the US is estimated to have the highest age-standardized incidence rate (902.71 per 100,000, 95% CI 375.44–2277.24), while Korea will have the lowest incidence rate (176.46 per 100,000, 95% CI 58.77–512.09) in 2030. A decrease in asthma incidence was observed in all countries with the overall AAPC ranging from -3.42% to -0.42%. Notably, a turning point was found around 2020, after which the incidence rates dropped significantly.</div></div><div><h3>Conclusions</h3><div>Pandemic-related factors may temporarily lower the incidence of asthma. The expected increasing asthma incidence in pre-COVID scenario (model 1) should still warrant attention from public health practitioners and call for efforts to reduce the burden of asthma.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 188-196"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324075","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}
Pub Date : 2024-09-01DOI: 10.1016/S2772-5588(24)00080-X
{"title":"Guide for Authors","authors":"","doi":"10.1016/S2772-5588(24)00080-X","DOIUrl":"10.1016/S2772-5588(24)00080-X","url":null,"abstract":"","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 200-210"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324077","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}
Idiopathic pulmonary fibrosis (IPF) is characterized by accumulation of myofibroblasts (MYFs) and extracellular matrix components, which leads to severe distortion and scarring of the gas exchange units of the lung, the alveoli, and ultimately respiratory failure. Fibrosis-associated MYFs are therefore widely regarded as the culprits that compromise the architectural makeup of the lung in fibrotic disease. During the past decade, the cellular source of MYFs has been intensely investigated. The rationale for such studies is that identifying the origin of these cells might help identify novel therapeutic targets and candidates to treat IPF patients. Recent advances in basic and translational research employing lineage tracing and multi-omics approaches have helped address the identity of MYF precursors, highlight the underlying heterogeneity, and to a less extent investigate MYF fate during fibrosis resolution. In this review, we discuss the current understanding of such important aspects of MYF biology as well as recent developments in the treatment of IPF.
{"title":"Understanding myofibroblast origin in the fibrotic lung","authors":"Mahsa Zabihi , Mahtab Shahriari Felordi , Arun Lingampally , Saverio Bellusci , Xuran Chu , Elie El Agha","doi":"10.1016/j.pccm.2024.08.003","DOIUrl":"10.1016/j.pccm.2024.08.003","url":null,"abstract":"<div><div>Idiopathic pulmonary fibrosis (IPF) is characterized by accumulation of myofibroblasts (MYFs) and extracellular matrix components, which leads to severe distortion and scarring of the gas exchange units of the lung, the alveoli, and ultimately respiratory failure. Fibrosis-associated MYFs are therefore widely regarded as the culprits that compromise the architectural makeup of the lung in fibrotic disease. During the past decade, the cellular source of MYFs has been intensely investigated. The rationale for such studies is that identifying the origin of these cells might help identify novel therapeutic targets and candidates to treat IPF patients. Recent advances in basic and translational research employing lineage tracing and multi-omics approaches have helped address the identity of MYF precursors, highlight the underlying heterogeneity, and to a less extent investigate MYF fate during fibrosis resolution. In this review, we discuss the current understanding of such important aspects of MYF biology as well as recent developments in the treatment of IPF.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 142-150"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324178","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}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.007
Justine V. Devulder
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease characterized by airflow limitation and changes in airway structures that can lead to chronic bronchitis, small airway diseases, and emphysema. COPD is the 3rd leading cause of death worldwide and despite current research, there are no curative disease treatments for COPD. As the prevalence of COPD is higher in people over 60 years old than in younger age groups, COPD is considered a condition of accelerated lung aging. Natural lung aging is associated with molecular, cellular, and physiological changes that cause alteration in lung structure, in lung function and regeneration, and decreased immune system response that could lead to lung disease like COPD. Mechanisms of accelerated lung aging are complex and composed by increased oxidative stress induced by exposure to cigarette smoke, by chronic inflammatory processes, and increased number of senescent cells within the airways. Cellular senescence is the cessation of cell division after a finite number of proliferation cycles or in response to cell stressors, such as oxidative stress. Senescent cells show activation of the cell cycle regulators p21CIP1 (cyclin-dependent kinase inhibitor-1), p16INK4 (cyclin-dependent kinase inhibitor-2A), and p53 (cellular tumor antigen p53) that lead to cell cycle arrest. Senescent cells exhibit a change in their phenotype and their metabolic activity, along with the production of proinflammatory proteins collectively known as senescence-associated secretory phenotype (SASP). This review aims to describe recent developments in our understanding of aging mechanisms and how the acceleration of lung aging participates in COPD pathophysiology and comorbidities. Understanding and targeting aging mechanisms may result in the development of new therapeutics that could be effective for COPD and also for other age-related diseases.
{"title":"Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development","authors":"Justine V. Devulder","doi":"10.1016/j.pccm.2024.08.007","DOIUrl":"10.1016/j.pccm.2024.08.007","url":null,"abstract":"<div><div>Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease characterized by airflow limitation and changes in airway structures that can lead to chronic bronchitis, small airway diseases, and emphysema. COPD is the 3<sup>rd</sup> leading cause of death worldwide and despite current research, there are no curative disease treatments for COPD. As the prevalence of COPD is higher in people over 60 years old than in younger age groups, COPD is considered a condition of accelerated lung aging. Natural lung aging is associated with molecular, cellular, and physiological changes that cause alteration in lung structure, in lung function and regeneration, and decreased immune system response that could lead to lung disease like COPD. Mechanisms of accelerated lung aging are complex and composed by increased oxidative stress induced by exposure to cigarette smoke, by chronic inflammatory processes, and increased number of senescent cells within the airways. Cellular senescence is the cessation of cell division after a finite number of proliferation cycles or in response to cell stressors, such as oxidative stress. Senescent cells show activation of the cell cycle regulators p21<sup>CIP1</sup> (cyclin-dependent kinase inhibitor-1), p16<sup>INK4</sup> (cyclin-dependent kinase inhibitor-2A), and p53 (cellular tumor antigen p53) that lead to cell cycle arrest. Senescent cells exhibit a change in their phenotype and their metabolic activity, along with the production of proinflammatory proteins collectively known as senescence-associated secretory phenotype (SASP). This review aims to describe recent developments in our understanding of aging mechanisms and how the acceleration of lung aging participates in COPD pathophysiology and comorbidities. Understanding and targeting aging mechanisms may result in the development of new therapeutics that could be effective for COPD and also for other age-related diseases.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 133-141"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324177","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}