Metabolism: clinical and experimental最新文献

{"title":"Aging and metabolism in HFpEF: Pathophysiology and therapeutic implications","authors":"Min Ye ,&nbsp;Shenghui Feng ,&nbsp;Zixuan Xu ,&nbsp;Wenfeng He ,&nbsp;Chen Liu ,&nbsp;Wengen Zhu","doi":"10.1016/j.metabol.2025.156460","DOIUrl":"10.1016/j.metabol.2025.156460","url":null,"abstract":"<div><div>Heart failure with preserved ejection fraction (HFpEF) is increasingly recognized as an age-predominant syndrome characterized by diastolic dysfunction despite preserved systolic performance. In the aged myocardium, fatty acid oxidation capacity declines, while glycolytic flux increases; however, impaired pyruvate oxidation limits mitochondrial glucose oxidation, resulting in suboptimal ATP yield per oxygen molecule and worsening energetic inefficiency. Mitochondrial deficits, marked by reduced biogenesis, NAD⁺ depletion related to reduced sirtuin activity and consequent hyperacetylation of oxidative enzymes, and impaired electron-transport capacity, further diminish bioenergetic reserve and elevate reactive oxygen species generation. Concurrently, inflammaging and proteostatic collapse promote chronic low-grade inflammation, misfolded protein accumulation, and myocardial fibrosis, collectively contributing to increased ventricular stiffness and progressive HFpEF development. Therapeutic strategies targeting these interconnected pathways show considerable promise. Preclinical studies suggest that interventions such as NAD⁺ precursor supplementation, mTORC1 inhibition, and β-hydroxybutyrate administration can ameliorate HFpEF-like phenotypes by improving mitochondrial efficiency and reducing inflammation. SGLT2 inhibitors and GLP-1 receptor agonists confer clinically proven benefits in HFpEF, likely via systemic metabolic reprogramming toward more oxygen-efficient substrates and attenuation of inflammation. This review underscores the critical role of aging-associated metabolic and mitochondrial derangements in HFpEF pathogenesis and highlights mechanistically tailored interventions as the next frontier in managing this challenging, age-related syndrome.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156460"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145695666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ALDH2 variants – a role in cardiometabolic syndrome","authors":"Guanghong Jia ,&nbsp;William P. Fay ,&nbsp;Christos S. Mantzoros ,&nbsp;Michael A. Hill","doi":"10.1016/j.metabol.2025.156466","DOIUrl":"10.1016/j.metabol.2025.156466","url":null,"abstract":"","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156466"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145743326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are GLP-1 receptor agonists associated with reduced atrial fibrillation risk? Analyzing data duplication and uncertainty","authors":"Lucas M. Barbosa ,&nbsp;Vinícius Martins Rodrigues Oliveira","doi":"10.1016/j.metabol.2025.156490","DOIUrl":"10.1016/j.metabol.2025.156490","url":null,"abstract":"","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156490"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ACSL family: Bridging fatty acid metabolism and cell death in cancer progression","authors":"Ziqi Yu ,&nbsp;Lifeng Zhang ,&nbsp;Bo Jiang ,&nbsp;Lu Zhang ,&nbsp;Minghui Chen ,&nbsp;Mei Song","doi":"10.1016/j.metabol.2025.156470","DOIUrl":"10.1016/j.metabol.2025.156470","url":null,"abstract":"<div><div>Fatty acids (FAs) are indispensable for cellular homeostasis and centered in anabolic and catabolic pathways that are tightly governed by long-chain acyl-CoA synthetases (ACSLs). These enzymes drive fatty acid β-oxidation (FAO) to generate energy, remodel cell membrane phospholipid composition to dictate ferroptosis susceptibility, coordinate steroidogenesis and eicosanoid biosynthesis, and mediate metabolic reprogramming, thus acting as a central nexus between FAs metabolism and cell death. Dysregulation of ACSLs across malignancies fosters oncogenic dependency on metabolic reprogramming, influencing tumor progression, immune modulation, and therapy resistance, offering a rationale for anticancer therapeutic opportunities. Here, we delineate the decisive roles of ACSLs in the metabolic fate of FAs and cell death execution. We dissect their tumorigenic mechanisms through metabolic rewiring and cell death modulation, with an emphasis on ACSLs-mediated crosstalk between ferroptosis and cancer immunity. Furthermore, we discuss the potential of ACSLs-targeted agents in tumor therapy and the treatment of ferroptosis-associated pathologies, offering actionable insights for clinical translation.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156470"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Emerging roles of arginine metabolism in skeletal health and disease” [Metabolism 2025 Nov 19:175:156451. / PMID: 41270967]","authors":"Sibo Wang ,&nbsp;Qian Ren ,&nbsp;Yansheng Huang ,&nbsp;Yibo Ma ,&nbsp;Xuefang Zhang ,&nbsp;Yuan Liu ,&nbsp;Baorong He ,&nbsp;Liang Yan","doi":"10.1016/j.metabol.2025.156464","DOIUrl":"10.1016/j.metabol.2025.156464","url":null,"abstract":"","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156464"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145705273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of hepatosteatosis by isarubrolone C through AMPK-dependent regulation of lipophagy and lipid metabolism","authors":"Bo Chen ,&nbsp;Yuan-yuan Ma ,&nbsp;Miao-qing Zhang ,&nbsp;Rui Zhang ,&nbsp;Shu-fen Li ,&nbsp;Lin-zhuan Wu ,&nbsp;Jing-pu Zhang","doi":"10.1016/j.metabol.2025.156487","DOIUrl":"10.1016/j.metabol.2025.156487","url":null,"abstract":"<div><div>Targeting autophagy and fatty acid metabolism may be two promising therapeutic strategies for treating metabolic dysfunction-associated steatotic liver disease (MASLD). Our previous research demonstrated the ability of isarubrolone C (IroC), a bioactive polycyclic tropoloalkaloid to induce autophagy. However, the effects and mechanisms of IroC on MASLD have yet to be explored. Here, we generated a steatosis cell model using a minimum essential medium containing oleic acid and palmitic acid (HFA) in HepG2 cells, and a zebrafish model of hepatic steatosis fed a high-fat diet (HFD), and explored the role and mechanism of IroC against hepatic steatosis. HFA and HFD exposure caused lipid accumulation, fatty acid oxidation (FAO) defect and high expression of lipogenesis genes, and IroC treatment reversed these steatosis-like features <em>in vitro</em> and in the liver of zebrafish with MASLD. Mechanistically, IroC increased AMPK phosphorylation that further phosphorylated ULK1, ACC, PPARα and full-length SREBP1, by which lipophagy and FAO damaged by HFA were recovered, expression of <em>de novo</em> lipogenesis genes reduced, including <em>fasn</em> and <em>scd1</em> expression <em>via</em> downregulation of SREBP-1 activity; and CD36 for FA transport was decreased by p-AMPK inhibition of PPARγ phosphorylation. Notably, IroC exhibited a high binding affinity to the AMPKα1β2γ1 isoform, as demonstrated by both molecular docking and surface plasmon resonance assay. Our work uncovers that IroC exerts an activator of AMPK, by which IroC can activate lipophagy and FAO, and inhibit lipogenesis and lipid deposition in hepatocytes. Thereby, IroC has the potential to serve as an effective agent in the management of MASLD.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156487"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Food preference wars: The glucoprivation menace","authors":"Vitor Ferreira ,&nbsp;Miguel López","doi":"10.1016/j.metabol.2025.156468","DOIUrl":"10.1016/j.metabol.2025.156468","url":null,"abstract":"","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156468"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liver cancer chronically exposed to palmitate acquires ferroptosis resistance via the downregulation of glutamine-driven hepcidin expression","authors":"Dong-Ho Kim ,&nbsp;Mi Kyung Kim ,&nbsp;Daehoon Kim ,&nbsp;Eun-Jun Kwon ,&nbsp;Jieun Shin ,&nbsp;Sebin Lee ,&nbsp;Bae-Gon Kang ,&nbsp;Jae Won Yun ,&nbsp;Jaebon Lee ,&nbsp;Hye Won Lee ,&nbsp;Byoung Kuk Jang ,&nbsp;Ghilsuk Yoon ,&nbsp;Kwang-Hyeon Liu ,&nbsp;Jun-Kyu Byun ,&nbsp;Yeon-Kyung Choi ,&nbsp;Keun-Gyu Park","doi":"10.1016/j.metabol.2025.156469","DOIUrl":"10.1016/j.metabol.2025.156469","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Immune checkpoint blockade (ICB) has revolutionized treatment of hepatocellular carcinoma (HCC), but its efficacy remains limited. Recent studies demonstrate that resistance to ferroptosis is a significant barrier to the success of ICB.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Ferroptosis was assessed by measuring C11-BODIPY fluorescence and 4-hydroxynonenal (4-HNE) staining. Epigenetic regulation of hepcidin under fatty acid-rich conditions in HCC cells was investigated through chromatin immunoprecipitation and histone methylation analyses. Clinical relevance was evaluated using ICB response datasets and analyses of tumor tissues from HCC patients.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;We demonstrate that prolonged exposure to high palmitate concentrations induces ferroptosis resistance in HCC cells by altering glutamine availability. Mechanistically, chronic exposure to palmitate and high-fat diet-feeding reduced glutamine-derived α-KG concentrations in HCC cells, leading to a H3K27me3-mediated reduction in &lt;strong&gt;hepcidin&lt;/strong&gt; and depletion of the intracellular labile iron pool, thereby promoting resistance to anti-programmed death-ligand 1 (anti-PD-L1)-induced ferroptosis. This resistance was reversed by the EZH2 inhibitor tazemetostat, which epigenetically restored hepcidin expression in both &lt;em&gt;in vitro&lt;/em&gt; and &lt;em&gt;in vivo&lt;/em&gt; models. Notably, tumor tissues from HCC patients exhibited high FFA levels, along with low levels of glutamine, &lt;strong&gt;hepcidin,&lt;/strong&gt; and iron, which correlated with shorter overall survival. H3K27me3-mediated suppression of hepcidin was further confirmed in patient cohorts.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Our study uncovers a previously unrecognized type of palmitate-induced metabolic reprogramming that confers resistance to ICB-induced ferroptosis on HCC, and propose a therapeutic strategy to overcome ferroptosis resistance under free fatty acid-rich conditions.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Abbreviations&lt;/h3&gt;&lt;div&gt;&lt;span&gt;&lt;div&gt;&lt;div&gt;&lt;table&gt;&lt;tbody&gt;&lt;tr&gt;&lt;td&gt;ICB&lt;/td&gt;&lt;td&gt;Immune checkpoint blockade&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;xCT&lt;/td&gt;&lt;td&gt;cystine/glutamate antiporter&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;CoQ10&lt;/td&gt;&lt;td&gt;coenzyme Q10&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;FSP1&lt;/td&gt;&lt;td&gt;ferroptosis suppressor protein 1&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;NADPH&lt;/td&gt;&lt;td&gt;nicotinamide adenine dinucleotide phosphate, reduced form&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;GSH&lt;/td&gt;&lt;td&gt;glutathione&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;GSSG&lt;/td&gt;&lt;td&gt;glutathione disulfide&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;HCC&lt;/td&gt;&lt;td&gt;hepatocellular carcinoma&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;AD&lt;/td&gt;&lt;td&gt;palmitate-adapted HCC cells&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;PI&lt;/td&gt;&lt;td&gt;propidium iodide&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;ROS&lt;/td&gt;&lt;td&gt;lipid reactive oxygen species&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;IKE&lt;/td&gt;&lt;td&gt;imidazole ketone erastin&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;GPX4&lt;/td&gt;&lt;td&gt;glutathione peroxidase-4&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;LIP&lt;/td&gt;&lt;td&gt;labile iron pool&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;SLC&lt;/td&gt;&lt;td&gt;solute carrier&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;NRF2&lt;/td&gt;&lt;td&gt;nuclear factor erythroid 2-related factor 2&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;FFA&lt;/td&gt;&lt;td&gt;free fatty acid&lt;/td&gt;&lt;/tr&gt;&lt;tr&gt;&lt;td&gt;LFD&lt;/td&gt;&lt;td&gt;l","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156469"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolomic aging clock predicts risk of different cardiovascular diseases in the UK Biobank","authors":"Guochang You ,&nbsp;Kangjie Wang ,&nbsp;Runnan Shen ,&nbsp;Xiong Chen ,&nbsp;Jinjin Jiang ,&nbsp;Yunhao Sun ,&nbsp;Dan Wu ,&nbsp;Jiatang Xu ,&nbsp;Kai Huang ,&nbsp;Chen Yao","doi":"10.1016/j.metabol.2025.156467","DOIUrl":"10.1016/j.metabol.2025.156467","url":null,"abstract":"<div><div>Current metabolomic aging clocks inadequately capture individual heterogeneity in biological aging trajectories, constraining their clinical utility. Here, we developed a metabolomic age clock in the UK Biobank (<em>n</em> = 196,790) using a comprehensive panel of 249 plasma metabolites. This framework was trained to predict phenotypic age (PhenoAge), a validated composite biomarker that integrates clinical chemistry across multiple systems, and was evaluated for its utility to predict incident cardiovascular diseases (CVDs) and dementia. We found that this new measure accurately predicted actual PhenoAge (Pearson's r = 0.90) and was significantly associated with the incidence of seven CVDs, including major adverse cardiovascular events, atherosclerotic cardiovascular disease, myocardial infarction, stroke, aortic stenosis, heart failure, and abdominal aortic aneurysm, but not dementia. Furthermore, metabolomic aging was associated with biological, physical, and cognitive age-related phenotypes, comprising telomere length, frailty index, and reaction time. Incorporating the metabolomic age clock with PREVENT (Predicting Risk of CVD Events) risk score modestly improved the performance, as measured by C-statistic and net reclassification index. Genetic analyses revealed 91 genomic loci and 168 genes (e.g., <em>SERPINA1</em>, <em>FADS</em> cluster), with tissue-enrichment analysis highlighting the liver's significant role in metabolic aging. By bridging metabolomic profiles with multisystem aging information, this framework provides a measure of biological aging that is associated with age-related functional status and cardiovascular risk.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156467"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145705560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic and immune dysfunction at the crossroads between type 1 diabetes and neurodegeneration","authors":"Francesca D'Addio ,&nbsp;Loredana Bucciarelli ,&nbsp;Maria Elena Lunati ,&nbsp;Paolo Fiorina","doi":"10.1016/j.metabol.2025.156471","DOIUrl":"10.1016/j.metabol.2025.156471","url":null,"abstract":"<div><div>A growing body of evidence suggests that neurogenerative disorders are increasingly common in individuals with type 1 diabetes (T1D) and should be considered part of the heterogeneous impairment of the nervous system linked to the T1D condition. The already established association between brain health and blood glucose metabolic control pushes to normalize glycemia in individuals with neurodegenerative diseases as well as in those with T1D. Normoglycemia has, indeed, been associated with reduced brain atrophy and preserved neuronal plasticity and function. Interestingly, immune dysregulation recently demonstrated in neurodegenerative diseases may be highly relevant given the autoimmune nature of T1D. Poor glycemic control and a disrupted immune response may act as common pathogenic mechanisms that increase the incidence of neurodegenerative disorders in individuals with T1D and may unveil new diagnostic and therapeutic paths for future clinical advancements. In this narrative review, we summarize new evidence showing that brain damage and cognitive dysfunction are linked to T1D and delineate the role of altered glycemic control, neuronal loss and immune dysregulation. We also discuss novel therapeutic approaches that target the aforementioned mechanisms and may help prevent the onset of neurodegenerative disorders in individuals with T1D.</div></div>","PeriodicalId":18694,"journal":{"name":"Metabolism: clinical and experimental","volume":"176 ","pages":"Article 156471"},"PeriodicalIF":11.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}