Journal of respiratory biology and translational medicine最新文献

{"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":"<p><p>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.</p>","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}

{"title":"State of the ART: Drug Screening Reveals Artesunate as a Promising Anti-Fibrosis Therapy.","authors":"Yujie Qiao, Jiurong Liang, Dianhua Jiang","doi":"10.70322/jrbtm.2024.10023","DOIUrl":"10.70322/jrbtm.2024.10023","url":null,"abstract":"<p><p>Fibrosis is a progressive pathological process that severely impairs normal organ function. Current treatments for fibrosis are extremely limited, with no curative approaches available. In a recent article published in <i>Cell</i>, Zhang and colleagues employed drug screening using ACTA2 reporter iPSC-derived cardiac fibroblasts and identified artesunate as a potent antifibrotic drug by targeting MD2/TLR4 signaling. This study provides new insights into strategies for exploiting existing drugs to treat fibrosis.</p>","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/PMC11800322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143384888","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":"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":"<p><p>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.</p>","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}

{"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":"<p><p>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.</p>","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}

{"title":"Enhanced Spatial Transcriptomics Analysis of Mouse Lung Tissues Reveals Cell-Specific Gene Expression Changes Associated with Pulmonary Hypertension.","authors":"Hanqiu Zhao, Xiaokuang Ma, Peng Chen, Bin Liu, Jing Wei, John Zhang, Ankit A Desai, Andrea L Frump, Olga Rafikova, Michael B Fallon, Shenfeng Qiu, Zhiyu Dai","doi":"10.70322/jrbtm.2025.10004","DOIUrl":"10.70322/jrbtm.2025.10004","url":null,"abstract":"<p><p>Spatial transcriptomics technologies have emerged as powerful tools for understanding cellular identity and function within the natural spatial context of tissues. Traditional transcriptomics techniques, such as bulk and single-cell RNA sequencing, lose this spatial information, which is critical for addressing many biological questions. Here, we present a protocol for high-resolution spatial transcriptomics using fixed frozen mouse lung sections mounted on 10X Genomics Xenium slides. This method integrates multiplexed fluorescent in situ hybridization (FISH) with high-throughput imaging to reveal the spatial distribution of mRNA molecules in lung tissue sections, allowing detailed analysis of gene expression changes in a mouse model of pulmonary hypertension (PH). We compared two tissue preparation methods, fixed frozen and fresh frozen, for compatibility with the Xenium platform. Our fixed frozen approach, utilizing a free-floating technique to mount thin lung sections onto Xenium slides at room temperature, preserved tissue integrity and maximized the imaging area, resulting in high-fidelity spatial transcriptomics data. Using a predesigned 379-gene mouse panel, we identified 40 major lung cell types. We detected key cellular changes in PH, including an increase in arterial endothelial cells (AECs) and fibroblasts, alongside a reduction in capillary endothelial cells (CAP1 and CAP2). Through differential gene expression analysis, we observed markers of endothelial-to-mesenchymal transition and fibroblast activation in PH lungs. High-resolution spatial mapping further confirmed increased arterialization in the distal microvasculature. These findings underscore the utility of spatial transcriptomics in preserving the native tissue architecture and enhancing our understanding of cellular heterogeneity in disease. Our protocol provides a reliable method for integrating spatial and transcriptomic data using fixed frozen lung tissues, offering significant potential for future studies in complex diseases such as PH.</p>","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144277320","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":"Surfactant Protein-C Regulates Alveolar Type 2 Epithelial Cell Lineages via the CD74 Receptor.","authors":"Krishan G Jain, Yang Liu, Runzhen Zhao, Preeti J Muire, Nan-Miles Xi, Hong-Long Ji","doi":"10.70322/jrbtm.2024.10017","DOIUrl":"10.70322/jrbtm.2024.10017","url":null,"abstract":"<p><strong>Background: </strong>Deficiency of surfactant protein-C (SPC) increases susceptibility to lung infections and injury, and suppressed expression of SPC has been associated with the severity of acute respiratory distress syndrome (ARDS). Alveolar type 2 epithelial cells (AT2) are critical for maintenance and repair of the lung. However, the role of the SPC in the regulation of AT2 cell lineage and the underlying mechanisms are not completely understood.</p><p><strong>Methods: </strong>This study aimed to investigate the mechanisms by which SPC regulates AT2 lineages. <i>Sftpc-/-</i> mice were used to model the SPC deficiency in ARDS patients. We utilized three-dimensional (3D) organoids to compare AT2 lineage characteristics between wild type (WT) and <i>Sftpc-/-</i> mice by analyzing AT2 proliferation, alveolar type 1 cells (AT1) differentiation and CD74 expression, using colony-formation assay, immunofluorescence, flow cytometry, and immunoblots.</p><p><strong>Results: </strong>The results showed that <i>Sftpc</i>-/- mice demonstrated a reduced AT2 cell population. Influenza A virus subtype H1N1 (H1N1) infected <i>Sftpc-/-</i> mice demonstrated reduced AT2 proliferation and AT1 differentiation. Western blot indicated elevated levels of CD74 protein in AT2 cells of <i>Sftpc-/-</i> mice. Colony-forming efficiency was significantly attenuated in AT2 cells isolated from <i>Sftpc-/-</i> mice compared to the WT controls. Podoplanin (PDPN, a marker of AT1 cells) expression and transient cell count significantly increased in <i>Sftpc-/-</i> organoids. Moreover, siRNA-mediated gene silencing of CD74 in AT2 cells significantly increased AT2 proliferation and AT1 differentiation in <i>Sftpc-/-</i> organoids.</p><p><strong>Conclusions: </strong>This study suggests that SPC regulates AT2 lineage in vitro and in vivo. The SPC might influence AT2 lineage during the lung epithelium repair by activating signaling mechanism involving CD74 receptor.</p>","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"1 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11565471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142650112","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":"The Interplay of Heart Failure and Lung Disease: Clinical Correlations, Mechanisms, and Therapeutic Implications.","authors":"Salma Ahmad, Ayman Isbatan, Sunny Chen, Steven M Dudek, Richard D Minshall, Jiwang Chen","doi":"10.70322/jrbtm.2024.10020","DOIUrl":"10.70322/jrbtm.2024.10020","url":null,"abstract":"<p><p>Heart failure (HF) is a common clinical syndrome marked by reduced cardiac output, elevated intracardiac pressures, and heart dysfunction. Chronic HF (CHF) is a syndrome characterized by a lack of blood flow and impaired pumping ability to the heart over time, while acute HF (AHF) arises suddenly due to incidents like myocardial infarction or cardiac arrest. HF has a significant impact on pulmonary health and function, leading to conditions such as pulmonary edema and restrictive lung patterns. Clinical evidence highlights the bidirectional relationship between HF and lung dysfunction. Declining lung function serves as a predictor for HF progression and severity, while HF contributes to worsening lung health. Animal models that induce HF through surgical methods further demonstrate the connection between heart and lung pathology. The main mechanisms linking HF and lung dysfunction are pressure overload and chronic systemic inflammation, with changes in the extracellular matrix (ECM) also playing a role. Additionally, environmental factors like air pollution exacerbate lung inflammation, increasing the risk of both HF and chronic obstructive pulmonary disease (COPD) incidence. Combined treatment approaches involving pharmaceutical drugs such as statins, Angiotensin-converting enzyme (ACE) inhibitors, and Angiotensin receptor blockers (ARBs) may benefit by reducing inflammation. This review will explore the complex interplay between HF and lung function, emphasizing their interconnected pathophysiology and potential integrated treatment strategies.</p>","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"1 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800330/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143367213","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":"Ion Channels in the Immune Response of Asthma.","authors":"Liang Yan, Lu Zhang, Kenneth Ogunniyi, Liang Hong","doi":"10.70322/jrbtm.2024.10019","DOIUrl":"10.70322/jrbtm.2024.10019","url":null,"abstract":"<p><p>Asthma is a common respiratory disorder characterized by chronic inflammation of the lower airways, contributing to significant morbidity, mortality, and a substantial global economic burden. It is now understood as a heterogeneous condition, with ongoing research shedding light on its complex immunological underpinnings. Ion channels, which are specialized transmembrane proteins that facilitate ion movement based on electrochemical gradients, play a crucial role in the pathophysiology of asthma. Ion channels regulate essential processes like maintaining epithelial hydroelectrolyte balance and also play a role in modulating immune responses involved in asthma. We discuss the connection between ion channel activity and immune regulation in asthma, focusing on ion channel regulation of immune cell behavior, airway hyperresponsiveness, and inflammation in asthma. Understanding ion channels in asthma could lead to the development of targeted therapies modulating their activity, thereby enhancing disease management and patient outcomes.</p>","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"1 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814969","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":"Diversity and Meta-Analysis of Microbial Differential Abundance in Nasal Metatranscriptomic Profiles of Asthma.","authors":"Andrew Li, Molin Yue, Xiangyu Ye, Kristina Gaietto, Anna F Wang-Erickson, Wei Chen","doi":"10.70322/jrbtm.2024.10018","DOIUrl":"10.70322/jrbtm.2024.10018","url":null,"abstract":"<p><p>Asthma affects millions worldwide and involves complex genetic, immunological, and environmental factors. The nasal microbiome is increasingly recognized for its role in asthma development, but inconsistent results and small sample sizes have limited a clear understanding. We aimed to clarify the nasal microbiome's role in asthma using large datasets and meta-transcriptomic analysis. RNA-seq data was analyzed from two large public studies: GALA II (694 children of Puerto Rican heritage; 441 asthmatics, 253 controls) and CAAPA (562 individuals of African ancestry; 265 asthmatics, 297 controls). After quality control and host read removal, microbial reads were annotated using Kraken2. α and β diversity analyses compared microbial diversity between asthmatic and control groups. Differential abundance analysis was conducted separately, controlling for age and sex, with results combined via meta-analysis. We found that asthmatic patients exhibited significantly higher α diversity indices (Shannon, Berger-Parker, Inverse Simpson, Fisher's) in nasal microbiota compared to controls in GALA II, with similar trends in CAAPA. β diversity analysis showed significant differences in microbial composition in GALA II data. Differential abundance analysis identified 20 species in GALA II and 9 species in CAAPA significantly associated with asthma. Meta-analysis revealed 11 species significantly associated with asthma, including <i>Mycobacterium_tuberculosis</i>. Our study demonstrates increased nasal microbiome α diversity in asthmatic patients and identifies specific microbial species associated with asthma risk. These findings enhance understanding of asthma pathogenesis from the nasal microbiome perspective and may inform future research and therapeutic strategies.</p>","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"1 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11600520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752674","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":"Sulforaphane's Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)-Dependent and -Independent Mechanism of Anti-SARS-CoV-2 Activity.","authors":"Ziqi Yan, Weifeng Liang, Lingxiang Zhu, Ivana Kreso, Venesa Romero, Melisa Smith, Yin Chen","doi":"10.35534/jrbtm.2024.10010","DOIUrl":"10.35534/jrbtm.2024.10010","url":null,"abstract":"<p><p>It is well established that Nrf2 plays a crucial role in anti-oxidant and anti-inflammatory functions. However, its antiviral capabilities remain less explored. Despite this, several Nrf2 activators have demonstrated anti-SARS-CoV-2 properties, though the mechanisms behind these effects are not fully understood. In this study, using two mouse models of SARS-CoV-2 infection, we observed that the absence of Nrf2 significantly increased viral load and altered inflammatory responses. Additionally, we evaluated five Nrf2 modulators. Notably, epigallocatechin gallate (EGCG), sulforaphane (SFN), and dimethyl fumarate (DMF) exhibited significant antiviral effects, with SFN being the most effective. SFN did not impact viral entry but appeared to inhibit the main protease (M^Pro) of SARS-CoV-2, encoded by the Nsp5 gene, as indicated by two protease inhibition assays. Moreover, using two Nrf2 knockout cell lines, we confirmed that SFN's antiviral activity occurs independently of Nrf2 activation <i>in vitro</i>. Paradoxically, <i>in vivo</i> tests using the MA30 model showed that SFN's antiviral function was completely lost in Nrf2 knockout mice. Thus, although SFN and potentially other Nrf2 modulators can inhibit SARS-CoV-2 independently of Nrf2 activation in cell models, their Nrf2-dependent activities might be crucial for antiviral defense under physiological conditions.</p>","PeriodicalId":517993,"journal":{"name":"Journal of respiratory biology and translational medicine","volume":"1 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11360660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142116785","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}