Journal of Clinical and Translational Hepatology最新文献

{"title":"Application of Cone-beam Computed Tomography in Interventional Therapies for Liver Malignancy: A Consensus Statement by the Chinese College of Interventionalists.","authors":"Bin-Yan Zhong, Zhong-Zhi Jia, Wen Zhang, Chang Liu, Shi-Hong Ying, Zhi-Ping Yan, Cai-Fang Ni, Clinical Guidelines Committee Of Chinese College Of Interventionalists","doi":"10.14218/JCTH.2024.00213","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00213","url":null,"abstract":"<p><p>Despite its crucial role in interventional therapies for liver malignancy, cone-beam computed tomography (CBCT) has not yet been fully integrated into clinical practice due to several complicating factors, including nonstandardized operations and limited recognition of CBCT among interventional radiologists. In response, the Chinese College of Interventionalists has released a consensus statement aimed at standardizing and promoting the application of CBCT in the interventional therapies for liver malignancy. This statement summarizes CBCT scanning techniques, and operational standards, and highlights its potential applications in clinical practice.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 10","pages":"886-891"},"PeriodicalIF":3.1,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11491508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142501223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High Levels of Vitamin C Intake Modify Effects of Phthalates on Metabolic Dysfunction-associated Steatotic Liver Disease: A Nationally Representative Study.","authors":"Ruoqi Zhou, Yuwei Wang, Xinxin Liu, Xia Yu, Dajing Xia, Yihua Wu, Yu Shi","doi":"10.14218/JCTH.2024.00186","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00186","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 10","pages":"892-895"},"PeriodicalIF":3.1,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11491502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142501279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison between Liver Cancer Mortality Rates in China and Spain.","authors":"Javier Guinea-Castañares, Jesus Maria Iturralde Iriso, Irune Natalia Elizondo Pinillos, Gloria Martinez Iniesta","doi":"10.14218/JCTH.2024.00219","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00219","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 10","pages":"831-833"},"PeriodicalIF":3.1,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11491503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142501224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and Validation of a New Prognostic Model for Predicting Survival Outcomes in Patients with Acute-on-chronic Liver Failure.","authors":"Wende Li, Wanshu Liu, Yihui Rong, Dongze Li, Bing Zhu, Shaobo Yang, Shidong Sun, Shaoli You, Yu Chen, Jun Li","doi":"10.14218/JCTH.2024.00316","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00316","url":null,"abstract":"<p><strong>Background and aims: </strong>Early determination of prognosis in patients with acute-on-chronic liver failure (ACLF) is crucial for optimizing treatment options and liver allocation. This study aimed to identify risk factors associated with ACLF and to develop new prognostic models that accurately predict patient outcomes.</p><p><strong>Methods: </strong>We retrospectively selected 1,952 hospitalized patients diagnosed with ACLF between January 2010 and June 2018. This cohort was used to develop new prognostic scores, which were subsequently validated in external groups.</p><p><strong>Results: </strong>The study included 1,386 ACLF patients and identified six independent predictors of 28-day mortality through multivariate analysis (all <i>p</i> < 0.05). The new score, based on a multivariate regression model, demonstrated superior predictive accuracy for both 28-day and 90-day mortalities, with Areas under the ROC curves of 0.863 and 0.853, respectively (all <i>p</i> < 0.05). This score can be used to stratify the risk of mortality among ACLF patients with ACLF, showing a significant difference in survival between patients categorized by the cut-off value (log-rank (Mantel-Cox) χ² = 487.574 and 606.441, <i>p</i> = 0.000). Additionally, the new model exhibited good robustness in two external cohorts.</p><p><strong>Conclusions: </strong>This study presents a refined prognostic model, the Model for end-stage liver disease-complication score, which accurately predicts short-term mortality in ACLF patients. This model offers a new perspective and tool for improved clinical decision-making and short-term prognostic assessment in ACLF patients.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 10","pages":"834-844"},"PeriodicalIF":3.1,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11491505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142501278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic Landscape Analysis Reveals a Persistent DNA Damage Response in Metabolic Dysfunction-associated Steatohepatitis Post-dietary Intervention.","authors":"Zi-Yuan Zou, Tian-Yi Ren, Jia-Qi Li, Ting-Ying Jiao, Meng-Yu Wang, Lei-Jie Huang, Shuang-Zhe Lin, Yuan-Yang Wang, Xiao-Zhen Guo, Ye-Yu Song, Rui-Xu Yang, Cen Xie, Jian-Gao Fan","doi":"10.14218/JCTH.2024.00111","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00111","url":null,"abstract":"<p><strong>Background and aims: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) and its more advanced form, metabolic dysfunction-associated steatohepatitis, have emerged as the most prevalent liver diseases worldwide. Currently, lifestyle modification is the foremost guideline-recommended management strategy for MASLD. However, it remains unclear which detrimental signals persist in MASLD even after disease remission. Thus, we aimed to examine the persistent changes in liver transcriptomic profiles following this reversal.</p><p><strong>Methods: </strong>Male C57BL/6J mice were divided into three groups: Western diet (WD) feeding, chow diet (CD) feeding, or diet reversal from WD to CD. After 16 weeks of feeding, RNA sequencing was performed on the mice's livers to identify persistent alterations characteristic of MASLD. Additionally, RNA sequencing databases containing high-fat diet-fed P53-knockout mice and human MASLD samples were utilized.</p><p><strong>Results: </strong>WD-induced MASLD triggered persistent activation of the DNA damage response (DDR) and its primary transcription factor, P53, long after the resolution of the hepatic phenotype through dietary reversal. Elevated levels of P53 might promote apoptosis, thereby exacerbating metabolic dysfunction-associated steatohepatitis, as they strongly correlated with hepatocyte ballooning, an indicator of apoptosis activation. Moreover, P53 knockout in mice led to downregulated expression of apoptosis signaling in the liver. Mechanistically, P53 may regulate apoptosis by transcriptionally activating the expression of apoptosis-enhancing nuclease (AEN). Consistently, P53, AEN, and the apoptosis process all exhibited persistently elevated expression and showed a strong inter-correlation in the liver following dietary reversal.</p><p><strong>Conclusions: </strong>The liver demonstrated upregulation of DDR signaling and the P53-AEN-apoptosis axis both during and after exposure to WD. Our findings provide new insights into the mechanisms of MASLD relapse, highlighting DDR signaling as a promising target to prevent MASLD recurrence.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 9","pages":"765-779"},"PeriodicalIF":3.1,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11393837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of Metabolic Dysfunction-associated Steatotic Liver Disease: Important role of lipid metabolism.","authors":"Xiaoxi Feng, Rutong Zhang, Zhenye Yang, Kaiguang Zhang, Jun Xing","doi":"10.14218/JCTH.2024.00019","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00019","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease, has a high global prevalence and can progress to metabolic dysfunction-associated steatohepatitis, cirrhosis, and hepatocellular carcinoma. The pathogenesis of MASLD is primarily driven by disturbances in hepatic lipid metabolism, involving six key processes: increased hepatic fatty acid uptake, enhanced fatty acid synthesis, reduced oxidative degradation of fatty acids, increased cholesterol uptake, elevated cholesterol synthesis, and increased bile acid synthesis. Consequently, maintaining hepatic lipid metabolic homeostasis is essential for effective MASLD management. Numerous novel molecules and Chinese proprietary medicines have demonstrated promising therapeutic potential in treating MASLD, primarily by inhibiting lipid synthesis and promoting lipid oxidation. In this review, we summarized recent research on MASLD, elucidated the molecular mechanisms by which lipid metabolism disorders contribute to MASLD pathogenesis, and discussed various lipid metabolism-targeted therapeutic approaches for MASLD.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 9","pages":"815-826"},"PeriodicalIF":3.1,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11393839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Rising Burden of Hepatocellular Carcinoma: Is the Gender Gap Narrowing?","authors":"James K H Ho, Prem H Thurairajah, Daniel Q Huang, Kristie H Fan","doi":"10.14218/JCTH.2024.00216","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00216","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 9","pages":"763-764"},"PeriodicalIF":3.1,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11393844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Iron Overload Triggers the SMAD Pathway and Induces Hepcidin Expression in Hepatocytes through SMURF1.","authors":"Taha Yazal, Chia-Yang Li","doi":"10.14218/JCTH.2024.00220","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00220","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 9","pages":"761-762"},"PeriodicalIF":3.1,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11393842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pipeline of New Drug Treatment for Non-alcoholic Fatty Liver Disease/Metabolic Dysfunction-associated Steatotic Liver Disease.","authors":"Ye Hu, Chao Sun, Ying Chen, Yu-Dong Liu, Jian-Gao Fan","doi":"10.14218/JCTH.2024.00123","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00123","url":null,"abstract":"<p><p>Given the global prevalence and rising incidence of metabolic dysfunction-associated steatotic liver disease (MASLD), the absence of licensed medications is striking. A deeper understanding of the heterogeneous nature of MASLD has recently contributed to the discovery of novel groups of agents and the potential repurposing of currently available medications. MASLD therapies center on four major pathways. Considering the close relationship between MASLD and type 2 diabetes, the first approach involves antidiabetic medications, including incretins, thiazolidinedione insulin sensitizers, and sodium-glucose cotransporter 2 inhibitors. The second approach targets hepatic lipid accumulation and the resultant metabolic stress. Agents in this group include peroxisome proliferator-activated receptor agonists (e.g., pioglitazone, elafibranor, saroglitazar), bile acid-farnesoid X receptor axis regulators (obeticholic acid), de novo lipogenesis inhibitors (aramchol, NDI-010976), and fibroblast growth factor 21/19 analogs. The third approach focuses on targeting oxidative stress, inflammation, and fibrosis. Agents in this group include antioxidants (vitamin E), tumor necrosis factor α pathway regulators (emricasan, pentoxifylline, ZSP1601), and immune modulators (cenicriviroc, belapectin). The final group targets the gut (IMM-124e, solithromycin). Combination therapies targeting different pathogenetic pathways may provide an alternative to MASLD treatment with higher efficacy and fewer side effects. This review aimed to provide an update on these medications.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 9","pages":"802-814"},"PeriodicalIF":3.1,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11393841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncolytic Virus Senecavirus A Inhibits Hepatocellular Carcinoma Proliferation and Growth by Inducing Cell Cycle Arrest and Apoptosis.","authors":"Tao Gong, Xiao Liu, Qingyuan Li, Donald R Branch, Melika Loriamini, Wenxian Wen, Yaoqiang Shi, Qi Tan, Bin Fan, Zhonghui Zhou, Yujia Li, Chunhui Yang, Shilin Li, Xiaoqiong Duan, Limin Chen","doi":"10.14218/JCTH.2024.00125","DOIUrl":"10.14218/JCTH.2024.00125","url":null,"abstract":"<p><strong>Background and aims: </strong>Hepatocellular carcinoma (HCC) is a highly aggressive tumor with limited treatment options and high mortality. Senecavirus A (SVA) has shown potential in selectively targeting tumors while sparing healthy tissues. This study aimed to investigate the effects of SVA on HCC cells <i>in vitro</i> and <i>in vivo</i> and to elucidate its mechanisms of action.</p><p><strong>Methods: </strong>The cell counting kit-8 assay and colony formation assay were conducted to examine cell proliferation. Flow cytometry and nuclear staining were employed to analyze cell cycle distribution and apoptosis occurrence. A subcutaneous tumor xenograft HCC mouse model was created <i>in vivo</i> using HepG2 cells, and Ki67 expression in the tumor tissues was assessed. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay and hematoxylin and eosin staining were employed to evaluate HCC apoptosis and the toxicity of SVA on mouse organs.</p><p><strong>Results: </strong><i>In vitro</i>, SVA effectively suppressed the growth of tumor cells by inducing apoptosis and cell cycle arrest. However, it did not have a notable effect on normal hepatocytes (MIHA cells). In an <i>in vivo</i> setting, SVA effectively suppressed the growth of HCC in a mouse model. SVA treatment resulted in a significant decrease in Ki67 expression and an increase in apoptosis of tumor cells. No notable histopathological alterations were observed in the organs of mice during SVA administration.</p><p><strong>Conclusions: </strong>SVA inhibits the growth of HCC cells by inducing cell cycle arrest and apoptosis. It does not cause any noticeable toxicity to vital organs.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 8","pages":"713-725"},"PeriodicalIF":3.1,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11310753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}