Chinese medical journal pulmonary and critical care medicine最新文献

{"title":"Understanding myofibroblast origin in the fibrotic lung","authors":"Mahsa Zabihi ,&nbsp;Mahtab Shahriari Felordi ,&nbsp;Arun Lingampally ,&nbsp;Saverio Bellusci ,&nbsp;Xuran Chu ,&nbsp;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}

{"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^rd 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^CIP1 (cyclin-dependent kinase inhibitor-1), p16^INK4 (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}

{"title":"Burden of RSV among inpatients with lower respiratory tract infection under 5 years of age: A 10-year retrospective study in Southwest China from 2009 to 2019","authors":"Taoyu Li ,&nbsp;Heping Fang ,&nbsp;Xiangyu Liu ,&nbsp;Yu Deng ,&nbsp;Na Zang ,&nbsp;Jun Xie ,&nbsp;Xiaohong Xie ,&nbsp;Zhengxiu Luo ,&nbsp;Jian Luo ,&nbsp;Yulin Liu ,&nbsp;Zhou Fu ,&nbsp;Luo Ren ,&nbsp;Enmei Liu","doi":"10.1016/j.pccm.2024.08.006","DOIUrl":"10.1016/j.pccm.2024.08.006","url":null,"abstract":"<div><h3>Objectives</h3><div>Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infection (LRTI). However, few comprehensive descriptions of the disease burden, medical resource utilization (MRU), and costs of RSV are available for China. This study aimed to provide the basis for the development of RSV prevention strategies by analyzing the burden of RSV among inpatients with lower respiratory tract infection under 5 years of age.</div></div><div><h3>Methods</h3><div>We conducted a retrospective hospital-based study from June 2009 to May 2019 in Chongqing. Inpatients with LRTI were tested for eight viruses. We analyzed the RSV disease burden, MRU, and direct hospitalization costs by using non-parametric Mann‒Whitney <em>U</em> test, Chi-squared test or Fisher's exact test and logistic regression.</div></div><div><h3>Results</h3><div>A total of 6991 children under 5 years of age with LRTI were included in this study. The overall RSV-positive rate was 34.5% (2410/6991). Prior to admission, 81.9% (1973/2410) of these RSV-positive cases were otherwise healthy. Compared with children aged 24–59 months, the odds ratio (OR) and 95% confidence interval (CI) for RSV infection were 2.509 (2.139–2.945), 1.882 (1.549–2.222), and 1.479 (1.240–1.765) for those aged 1–5 months, 6–11 months, and 12–23 months, respectively. The proportions of patients treated with invasive ventilation and continuous positive airway pressure (CPAP) were significantly higher among RSV-positive cases (1.1% [27/2410] and 3.9% [93/2410]) than RSV-negative cases (0.9% [43/4581] and 2.7% [124/4581]) (<em>P</em> = 0.023). Compared with RSV-negative cases, RSV-positive cases had significantly longer hospital length of stay (6 [5, 8] days <em>vs.</em> 6 [5, 8] days, <em>P</em> &lt; 0.001) and higher hospitalization costs (963.0 [757.9, 1298.5] USD <em>vs.</em> 935.6 [719.7, 1296.3] USD, <em>P</em> = 0.022).</div></div><div><h3>Conclusions</h3><div>Most RSV infections occurred during early childhood and among individuals in the otherwise healthy group. Younger age was associated with a higher RSV-positive rate. Effective prevention measures are needed in the earliest stages to reduce the RSV burden.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 182-187"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324181","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}

{"title":"Screening for viruses in lung adenocarcinoma in China","authors":"Zhuxing Chen ,&nbsp;Peng Liang ,&nbsp;Haoxiang Xu ,&nbsp;Shengli Yang ,&nbsp;Jilong Liu ,&nbsp;Shifu Chen ,&nbsp;Ran Zhong ,&nbsp;Akira Sugimoto ,&nbsp;Wenhua Liang ,&nbsp;Jianxing He ,&nbsp;Tomoya Kawaguchi","doi":"10.1016/j.pccm.2024.05.001","DOIUrl":"10.1016/j.pccm.2024.05.001","url":null,"abstract":"","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 197-199"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324076","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}

{"title":"Mechanisms of pulmonary endothelial barrier dysfunction in acute lung injury and acute respiratory distress syndrome","authors":"Yunchao Su ,&nbsp;Rudolf Lucas ,&nbsp;David J.R. Fulton ,&nbsp;Alexander D. Verin","doi":"10.1016/j.pccm.2024.04.002","DOIUrl":"10.1016/j.pccm.2024.04.002","url":null,"abstract":"<div><p>Endothelial cells (ECs) form a semi-permeable barrier between the interior space of blood vessels and the underlying tissues. Pulmonary endothelial barrier integrity is maintained through coordinated cellular processes involving receptors, signaling molecules, junctional complexes, and protein-regulated cytoskeletal reorganization. In acute lung injury (ALI) or its more severe form acute respiratory distress syndrome (ARDS), the loss of endothelial barrier integrity secondary to endothelial dysfunction caused by severe pulmonary inflammation and/or infection leads to pulmonary edema and hypoxemia. Pro-inflammatory agonists such as histamine, thrombin, bradykinin, interleukin 1β, tumor necrosis factor α, vascular endothelial growth factor, angiopoietin-2, and platelet-activating factor, as well as bacterial toxins and reactive oxygen species, cause dynamic changes in cytoskeletal structure, adherens junction disorganization, and detachment of vascular endothelial cadherin (VE-cadherin) from the actin cytoskeleton, leading to an increase in endothelial permeability. Endothelial interactions with leukocytes, platelets, and coagulation enhance the inflammatory response. Moreover, inflammatory infiltration and the associated generation of pro-inflammatory cytokines during infection cause EC death, resulting in further compromise of the structural integrity of lung endothelial barrier. Despite the use of potent antibiotics and aggressive intensive care support, the mortality of ALI is still high, because the mechanisms of pulmonary EC barrier disruption are not fully understood. In this review, we summarized recent advances in the studies of endothelial cytoskeletal reorganization, inter-endothelial junctions, endothelial inflammation, EC death, and endothelial repair in ALI and ARDS, intending to shed some light on the potential diagnostic and therapeutic targets in the clinical management of the disease.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 80-87"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000239/pdfft?md5=802c146601b1c651c521e1e7335e741b&pid=1-s2.0-S2772558824000239-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141390171","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}

{"title":"Association of ratios of visceral fat area/subcutaneous fat area and muscle area/standard body weight at T12 CT level with the prognosis of acute respiratory distress syndrome","authors":"Hui Shen ,&nbsp;Ying He ,&nbsp;Fan Lu ,&nbsp;Xiaoting Lu ,&nbsp;Bining Yang ,&nbsp;Yi Liu ,&nbsp;Qiang Guo","doi":"10.1016/j.pccm.2024.05.004","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.05.004","url":null,"abstract":"<div><h3>Background</h3><p>It is well-known that body composition metrics can influence the prognosis of various diseases. This study investigated how body composition metrics predict acute respiratory distress syndrome (ARDS) prognosis, focusing on the ratio of visceral fat area (VFA) to subcutaneous fat area (SFA), SFA to standard body weight (SBW), VFA to SBW, and muscle area (MA) to SBW. These metrics were assessed at the level of the twelfth thoracic vertebra (T12 computed tomography [CT] level) to determine their correlation with the outcomes of ARDS. The goal was to utilize these findings to refine and personalize treatment strategies for ARDS.</p></div><div><h3>Methods</h3><p>Patients with ARDS admitted to the intensive care units (ICUs) of three hospitals from January 2016 to July 2023 were enrolled in this study. Within 24 hours of ARDS onset, we obtained chest CT scans to measure subcutaneous fat, visceral fat, and muscle area at the T12 level. We then compared these ratios between survivors and non-survivors. Logistic regression was employed to identify prognostic risk factors. Receiver operating characteristic (ROC) curve analysis was utilized to determine the optimal cutoff for predictors of in-hospital mortality. Based on this cutoff, patients with ARDS were stratified. To reduce confounding factors, 1:1 propensity score matching (PSM) was applied. We conducted analyses of clinical feature and prognostic differences pre- and post-PSM between the stratified groups. Additionally, Kaplan–Meier survival curves were generated to compare the survival outcomes of these groups.</p></div><div><h3>Results</h3><p>Of 258 patients with ARDS, 150 survived and 108 did not. Non-survivors had a higher VFA/SFA ratio (<em>P</em> &lt;0.001) and lower SFA/SBW and MA/SBW ratios (both <em>P</em> &lt;0.001). Key risk factors were high VFA/SFA ratio (OR=2.081; <em>P</em>=0.008), age, acute physiology and chronic health evaluation (APACHE) II score, and lactate levels, while MA/SBW and albumin were protective. Patients with a VFA/SFA ratio ≥0.73 were associated with increased mortality, while those with an MA/SBW ratio &gt;1.55 cm²/kg had lower mortality, both pre- and post-PSM (<em>P</em>=0.001 and <em>P</em> &lt;0.001, respectively). Among 170 patients with pulmonary-origin ARDS, 87 survived and 83 did not. The non-survivor group showed a higher VFA/SFA ratio (<em>P</em> &lt;0.001) and lower SFA/SBW and MA/SBW (<em>P</em>=0.003, <em>P</em> &lt;0.001, respectively). Similar risk and protective factors were observed in this cohort. For VFA/SFA, a value above the cutoff of 1.01 predicted higher mortality, while an MA/SBW value below the cutoff of 1.48 cm²/kg was associated with increased mortality (both <em>P</em> &lt;0.001 pre-/post-PSM).</p></div><div><h3>Conclusions</h3><p>Among all patients with ARDS, the VFA to SFA ratio, MA to SBW ratio at the T12 level, age, APACHE II score, and lactate levels emerged as independent risk factors for mortality.</p></di","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 106-118"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000331/pdfft?md5=e38d7a175826b55b02d8aa8234eef2e7&pid=1-s2.0-S2772558824000331-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141480123","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}

{"title":"Understanding cachexia and its impact on lung cancer and beyond","authors":"Meiting Yue ,&nbsp;Zhen Qin ,&nbsp;Liang Hu ,&nbsp;Hongbin Ji","doi":"10.1016/j.pccm.2024.02.003","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.02.003","url":null,"abstract":"<div><p>Cancer cachexia is a multifactorial syndrome characterized by loss of body weight secondary to skeletal muscle atrophy and adipose tissue wasting. It not only has a significant impact on patients’ quality of life but also reduces the effectiveness and tolerability of anticancer therapy, leading to poor clinical outcomes. Lung cancer is a prominent global health concern, and the prevalence of cachexia is high among patients with lung cancer. In this review, we integrate findings from studies of lung cancer and other types of cancer to provide an overview of recent advances in cancer cachexia. Our focus includes topics such as the clinical criteria for diagnosis and staging, the function and mechanism of selected mediators, and potential therapeutic strategies for clinical application. A comprehensive summary of current studies will improve our understanding of the mechanisms underlying cachexia and contribute to the identification of high-risk patients, the development of effective treatment strategies, and the design of appropriate therapeutic regimens for patients at different disease stages.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 95-105"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000045/pdfft?md5=6b4623cf381c108a5969dd91be15c0e4&pid=1-s2.0-S2772558824000045-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141479693","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}

{"title":"Cell–cell interactions and communication dynamics in lung fibrosis","authors":"Ting Xie,&nbsp;Jiurong Liang,&nbsp;Barry Stripp,&nbsp;Paul W. Noble","doi":"10.1016/j.pccm.2024.04.001","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.04.001","url":null,"abstract":"<div><p>Cell–cell interactions are essential components of coordinated cell function in lung homeostasis. Lung diseases involve altered cell–cell interactions and communication between different cell types, as well as between subsets of cells of the same type. The identification and understanding of intercellular signaling in lung fibrosis offer insights into the molecular mechanisms underlying these interactions and their implications in the development and progression of lung fibrosis. A comprehensive cell atlas of the human lung, established with the facilitation of single-cell RNA transcriptomic analysis, has enabled the inference of intercellular communications using ligand–receptor databases. In this review, we provide a comprehensive overview of the modified cell–cell communications in lung fibrosis. We highlight the intricate interactions among the major cell types within the lung and their contributions to fibrogenesis. The insights presented in this review will contribute to a better understanding of the molecular mechanisms underlying lung fibrosis and may guide future research efforts in developing targeted therapies for this debilitating disease.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 63-71"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000252/pdfft?md5=02e0ead30d3d12cef2311866a3340fdc&pid=1-s2.0-S2772558824000252-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141479694","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}

{"title":"Prevalence of nicotine dependence among smokers aged 40 years and older in China","authors":"Ying Ji ,&nbsp;Shu Cong ,&nbsp;Jing Fan ,&nbsp;Ning Wang ,&nbsp;Wenjing Wang ,&nbsp;Xuping Song ,&nbsp;Liwen Fang","doi":"10.1016/j.pccm.2024.05.003","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.05.003","url":null,"abstract":"<div><h3>Background</h3><p>Nicotine dependence, also known as tobacco dependence, is a common chronic disease and a major risk factor for chronic respiratory diseases. The present study was designed to determine the prevalence of nicotine dependence and its changes among smokers aged 40 years and older in China, to analyze the characteristics of nicotine dependence among smokers, and to provide a reference for smoking cessation interventions.</p></div><div><h3>Methods</h3><p>The data were sourced from nationally representative large-sample surveys conducted during 2014–2015 and 2019–2020 in the Chinese population, covering 125 counties (districts) in 31 provinces, autonomous regions and municipalities. Variables related to smoking and nicotine dependence among residents ≥40 years old were collected in face-to-face interviews. A total of 20,062 and 18,975 daily smokers were included in the 2014–2015 and 2019–2020 surveys, respectively. The severity of nicotine dependence was evaluated according to the Fagerström Test for Nicotine Dependence and Heaviness of Smoking Index. The level and change in nicotine dependence among daily smokers aged ≥40 years were estimated using a complex weighted sampling design, and their influencing factors were analyzed.</p></div><div><h3>Results</h3><p>Levels of nicotine dependence among daily smokers aged ≥40 years in China could be divided into very low, low, medium, high, and very high, accounting for 31.1%, 27.9%, 13.4%, 20.5%, and 7.1% of the total, respectively. The average Fagerström Test for Nicotine Dependence score was 3.9 (95% confidence interval [CI]: 3.8–4.0), with the prevalence of medium–high nicotine dependence being 41.0% (95% CI: 39.0–42.9%) and that of high and very high nicotine dependence being 27.6% (95% CI: 26.0–29.3%), both of which were significantly higher in men than in women (both <em>P</em> &lt; 0.001). Among daily smokers, those with a low education level, age at smoking initiation &lt;18 years, and with smoking duration of ≥20 years had a higher degree of nicotine dependence. In terms of geographic region, the level of medium–high nicotine dependence in South China was higher than in other areas, and the decline in the prevalence of high nicotine dependence was the greatest in Northwest China (<em>P</em> &lt; 0.001). The prevalence of medium–high and high and very high nicotine dependence was significantly higher in men with chronic respiratory symptoms, chronic obstructive pulmonary disease (COPD), and/or chronic respiratory diseases than in men without these conditions (all <em>P</em> &lt; 0.05). The prevalence of high and very high nicotine dependence in women with chronic respiratory symptoms and chronic respiratory diseases was significantly higher than that in women without these conditions (both <em>P</em> &lt; 0.05). Compared with that during 2014–2015, the prevalence of high nicotine dependence among daily smokers decreased during 2019–2020 by 4.5 percentage points in the total ","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 119-131"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S277255882400032X/pdfft?md5=e325d93d5c1aef7ba786643c409d2ec5&pid=1-s2.0-S277255882400032X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141479691","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}

{"title":"Biomarkers in idiopathic pulmonary fibrosis: Current insight and future direction","authors":"Zhen Zheng,&nbsp;Fei Peng,&nbsp;Yong Zhou","doi":"10.1016/j.pccm.2024.04.003","DOIUrl":"10.1016/j.pccm.2024.04.003","url":null,"abstract":"<div><p>Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease with a dismal prognosis. Early diagnosis, accurate prognosis, and personalized therapeutic interventions are essential for improving patient outcomes. Biomarkers, as measurable indicators of biological processes or disease states, hold significant promise in IPF management. In recent years, there has been a growing interest in identifying and validating biomarkers for IPF, encompassing various molecular, imaging, and clinical approaches. This review provides an in-depth examination of the current landscape of IPF biomarker research, highlighting their potential applications in disease diagnosis, prognosis, and treatment response. Additionally, the challenges and future perspectives of biomarker integration into clinical practice for precision medicine in IPF are discussed.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 72-79"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000240/pdfft?md5=381b53fe7d1a86f6287eea01a6e1c1aa&pid=1-s2.0-S2772558824000240-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141409116","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}