中华肝脏病杂志最新文献

{"title":"[Menstrual blood-derived mesenchymal stem cell transplantation improves anti-fibrosis mechanisms in mouse models of alcoholic liver fibrosis].","authors":"C Yang, A Li, Y Gao, M Q Wu, Z Y Wei, J Y Cui, Z Y Xu, T Wu","doi":"10.3760/cma.j.cn501113-20251011-00428","DOIUrl":"10.3760/cma.j.cn501113-20251011-00428","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the ameliorative effect of menstrual blood-derived mesenchymal stem cells (MenSCs) on liver fibrosis and injury, and further study whether it plays a role by regulating the Toll-like receptor (TLR) signaling pathway in a mouse model of alcoholic liver disease (ALD). <b>Methods:</b> A C57BL/6J mouse model of ALD was established using the gradient ethanol gavage method combined with pyrazole. A blank control group and a model group were established. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) activities, as well as inflammatory factors, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), were measured. The modeling effect was evaluated by combining Masson staining and Sirius red staining in liver tissue with Western blotting to detect the protein expression of α-smooth muscle actin (α-SMA) and collagen type I α1 chain (COL1A1). Simultaneously, qPCR was used to detect the mRNA expression of TLRs and transforming growth factor β-activated kinase 1 (TAK1) to explore the related mechanisms. ALD model mice were divided into a phosphate-buffered saline (PBS) control group and a MenSCs treatment group [2×10⁵ MenSCs (200 μL) injected via tail vein], with intervention once a week sustained for four weeks after successful modeling. Mice batches were sacrificed on the seventh day following each intervention to collect serum and liver tissues. Collagen deposition changes were observed using Sirius red staining. The expression of α-SMA and transforming growth factor-β1 (TGF-β1) proteins was detected by Western blotting. Serum biochemical indicators levels were also measured. The effects of MenSCs on TLRs and TAK1 mRNA expression were assessed using qPCR to comprehensively evaluate the MenSCs intervention effect. The two groups were compared using paired <i>t</i>-tests. Repeated measures analysis of variance (RM-ANOVA) combined with Tukey's multiple comparisons test was used for comparisons among multiple groups. <b>Results:</b> Compared with the blank control group, serum levels of ALT, AST, and GGT, as well as inflammatory factors TNF-α and IL-6, were significantly elevated, while IL-1β levels were significantly decreased in the mouse model of the ALD group. Collagen deposition in liver tissue was markedly increased. The expression of fibrosis markers α-SMA and COL1A1 proteins was significantly upregulated (α-SMA: <i>P</i><0.001; COL1A1: <i>P</i><0.001). The mRNA expression of TLR1, TLR2, TLR4, TLR6, TLR7, and TLR8 was significantly upregulated, and the expression of TLR9 and TAK1 was downregulated, while the expression of TLR3 and TLR5 remained unchanged. Liver function levels (ALT and AST) were significantly reduced; liver fibrosis degree was markedly improved; and TGF-β1 and α-SMA protein expression were suppressed (TGF-β1: <i>P</i><0.001; α-SMA: <i>P</i>=0.026) following MenSC transplantation in mice. MenSC specif","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 5","pages":"456-466"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057038","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":"[Analysis of familial intrahepatic cholestasis caused by ubiquitin-specific peptidase 53 gene mutation].","authors":"H Wang, X Zheng, M M Yu, Z D Yu, Y S Wang","doi":"10.3760/cma.j.cn501113-20250902-00360","DOIUrl":"10.3760/cma.j.cn501113-20250902-00360","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the clinical characteristics and gene mutation status of progressive familial intrahepatic cholestasis caused by a ubiquitin-specific peptidase 53 (USP53) gene mutation (USP53-FIC) in a family. <b>Methods:</b> A female infant patient with USP53-FIC and her family who presented to the Department of Gastroenterology, Children's Hospital Affiliated with Zhengzhou University, in May 2025 with a one-month history of jaundice and yellow urine, which worsened over a one-week period of ecchymosis, were selected as the study subjects. Peripheral blood samples were collected from the patient, her parents, and her elder brother for whole-exome sequencing of the family, followed by Sanger sequencing for validation. <b>Results:</b> The patient was a 5-month-23-day-old female presenting primarily with jaundice of the skin and sclera, dark urine, and skin ecchymosis. Liver function tests indicated cholestasis, normal gamma-glutamyl transferase, and abnormal coagulation function. Whole-exome sequencing of the family revealed a compound heterozygous variant of c.1558C>T and c.829dup in the USP53 gene, inherited from her mother and father, respectively. Sanger sequencing confirmed that the patient's older brother carried the same variants. The c.1558C>T was previously reported as a pathogenic variant, while c.829dup was previously unreported. PVS1 + PM2_Supporting + PM3 was reported as a pathogenic variant according to the American Society for Medical Genetics and Genomics variant rating guidelines. <b>Conclusion:</b> The compound heterozygous variant c.1558C>T and c.829dup in the USP53 gene are the genetic cause of this USP53-FIC in a family. USP53-FIC should be suspected for infants who suddenly develop cholestasis accompanied by coagulation disorders but normal gamma-glutamyl transferase levels. Genetic testing is helpful in clarifying the diagnosis and guiding treatment. The c.829dup variant enriches the variant spectrum of the USP53 gene.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 5","pages":"476-481"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148056976","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":"[Pathophysiological mechanisms of coagulation dysfunction associated with liver disease].","authors":"H Wang, X Chen, Y Y Lu","doi":"10.3760/cma.j.cn501113-20260204-00056","DOIUrl":"10.3760/cma.j.cn501113-20260204-00056","url":null,"abstract":"<p><p>Coagulation abnormalities associated with liver diseases easily lead to spontaneous and secondary bleeding, which is associated with hemodynamic changes, reduced synthesis of coagulation factors, liver disease-related thrombocytopenia, and pharmacological interventions. On the other hand, patients with liver disease also have a hypercoagulable state, making them prone to portal vein thrombosis, which is associated with hemodynamic changes, reduced synthesis of anticoagulants, abnormal vascular intima structure, inflammation, and pharmacological treatment. Additionally, patients with liver disease are at an intertwined risk of bleeding and thrombosis and are in a fragile state of hemostasis rebalancing for an extended period. Genetic factors and diagnostic and therapeutic procedures further challenge the management of coagulation function in patients with liver disease. This article discusses the mechanisms of coagulation abnormalities from the perspectives of both bleeding and thrombosis, providing assistance for dynamically managing and rebalancing the hemostasis in patients with liver disease.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 5","pages":"486-493"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057200","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":"[Research progress on cellular senescence and liver diseases].","authors":"L T Zhang, J M Hu, J W Wang, H Li, Y J Qin","doi":"10.3760/cma.j.cn501113-20251219-00540","DOIUrl":"10.3760/cma.j.cn501113-20251219-00540","url":null,"abstract":"<p><p>Cellular senescence, a stable state of proliferative arrest induced by stressors such as telomere shortening and DNA damage, is often accompanied by a senescence-associated secretory phenotype (SASP) that is closely related to the imbalance of liver homeostasis and the progression of chronic liver diseases. This article outlines the main phenotypes and signaling pathways of cellular senescence, reviews research progress on the senescence of different liver cell populations and the senescence-associated secretory phenotype in metabolic-associated fatty liver disease, viral hepatitis, liver fibrosis/cirrhosis, and hepatocellular carcinoma, discusses their \"double-edged sword\" effects at different etiologies and stages, and summarizes intervention strategies such as senolytic drugs and their potential in combination with antiviral, antifibrotic, and immunotherapy. Concurrently, it also points out needs still to be established unifying evaluation system and translatable biomarkers.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 5","pages":"502-510"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057184","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":"[Expert consensus on the clinical diagnosis and treatment of coagulation disorders related to liver disease].","authors":"","doi":"10.3760/cma.j.cn501113-20260203-00055","DOIUrl":"10.3760/cma.j.cn501113-20260203-00055","url":null,"abstract":"<p><p>Coagulation disorders are a major contributing factor to bleeding and thrombotic diseases in patients with liver disease. Furthermore, it is one of the severe complications, which is closely related to disease progression and poor prognosis, affecting various diagnostic and therapeutic procedures in patients with liver disease. Therefore, accurately assessing the coagulation function, maintaining the balance of their coagulation status, and establishing clinical diagnostic and treatment standards for the prevention and treatment of bleeding and thrombosis are of great significance for the liver disease patients' clinical diagnosis and treatment. This consensus is formulated in discussion with experts from fields in hepatology, hematology, critical care medicine, laboratory medicine, and clinical pharmacy in reference to the latest evidence-based medicine with the aim of providing guidance for the clinical diagnosis and treatment of coagulation disorder in patients with liver disease.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 5","pages":"417-429"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057035","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":"[An excerpt of the European Association for the Study of the Liver's clinical practice guidelines on liver vascular diseases in 2025].","authors":"B H Luo, G H Han","doi":"10.3760/cma.j.cn501113-20251226-00550","DOIUrl":"10.3760/cma.j.cn501113-20251226-00550","url":null,"abstract":"<p><p>Liver vascular diseases include portal vein thrombosis (with or without cirrhosis), portal-sinusoidal vascular disease, Budd-Chiari syndrome, hepatic sinusoidal obstruction syndrome, non-obstructive sinusoidal dilatation and peliosis hepatis, visceral artery aneurysms, and hepatic arteriovenous fistulas. Importantly, with the exception of portal vein thrombosis in cirrhosis, the others are rare conditions. A substantial body of evidence has been published on the diagnosis, pharmacological treatment, and interventional therapy of liver vascular disorders since the European Association for the Study of the Liver issued the previous version of the clinical practice guidelines in 2016. These guidelines are based on a comprehensive review of relevant literature, providing recommendations for key clinical challenges and emphasizing implementation of individualized treatment by combining individual risk factors and clinical presentations. Thus, multidisciplinary collaborative management involving hepatologists, hematologists, pathologists, interventional radiologists, and surgeons is crucial in this field. The aim of this guideline is to provide guidance for the management of liver vascular diseases based on the best available evidence.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 5","pages":"443-455"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057004","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":"[Expert recommendations on the management of adverse reactions in pegylated interferon alpha therapy for chronic hepatitis B].","authors":"","doi":"10.3760/cma.j.cn50113-20260122-00037","DOIUrl":"10.3760/cma.j.cn50113-20260122-00037","url":null,"abstract":"<p><p>To provide a usage reference for clinicians with the increasing use of pegylated interferon alpha (PEG-IFN-ɑ) in treating chronic hepatitis B (CHB), the expert panel retrospectively summarized previous clinical experience and formulated expert recommendations based on the latest research findings and evidence-based medical data of this field, focusing on pre-treatment assessment to better assist clinicians in managing adverse reactions, help patients complete treatment courses, and maximize patient benefits.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 5","pages":"430-437"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057025","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":"[Study on the establishment, assessment, and drug sensitivity testing for intrahepatic cholangiocarcinoma organoid models based on the suspension culture method].","authors":"Y H Su, W Huang, C Yu, Y R Liu, P R Wu, C P Chai, L Li, H Xu, W C Zhou","doi":"10.3760/cma.j.cn501113-20250414-00140","DOIUrl":"10.3760/cma.j.cn501113-20250414-00140","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the feasibility of establishing intrahepatic cholangiocarcinoma (ICC) organoid models based on the suspension culture method. <b>Methods:</b> Fresh tumor tissue specimens were prepared from six patients with intrahepatic cholangiocarcinoma using digestive enzymes for a cell suspension. The cells were cultured as organoids in ultra-low attachment plates. Passaging and cryopreservation were used once the organoids reached an appropriate size. The formation of the organoids was monitored and recorded using an inverted microscope during the culture process. The organoids were collected and detected by hematoxylin-eosin staining and immunohistochemistry. The protein expressional conditions were examined. <b>Results:</b> Stable passaged and cryopreserved organoids from three tumor tissue samples were successfully constructed. Hematoxylin-eosin staining results showed that the organoids were structurally similar to the primary tissue. Immunohistochemical staining results demonstrated that CK7, CK19, E-cadherin, and vimentin were all positively expressed, with Ki67 positivity rates of approximately 50%, 30%, and 80%, respectively. <b>Conclusion:</b> The suspension culture method can construct organoid models in terms of tissue structure and protein expression that exhibit tumor characteristics of intrahepatic cholangiocarcinoma.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 4","pages":"340-347"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783227","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":"[Research advances of magnetic resonance elastography for assessing the bioinvasiveness in hepatocellular carcinoma].","authors":"M Y Ma, R K Li","doi":"10.3760/cma.j.cn501113-20250406-00124","DOIUrl":"10.3760/cma.j.cn501113-20250406-00124","url":null,"abstract":"<p><p>The invasiveness of hepatocellular carcinoma (HCC) is closely correlated with the dynamic changes in the biomechanical microenvironment. The solid (e.g., tissue sclerosis due to stromal fibrosis) and fluid mechanics processes (e.g., disordered interstitial hydraulic gradient) of HCC are significantly aberrant in comparison to normal liver tissue. These mechanical characteristics synergistically promote tumor invasion and metastasis by regulating mechanosensitive pathways and forming an interaction network with key biochemical signals. Magnetic resonance elastography (MRE), as a non-invasive technique, enables quantitative assessment of the mechanical heterogeneity of HCC by accurately characterizing tissue viscoelastic indices (e.g., shear modulus and loss modulus). Several studies have confirmed that MRE parameters are strongly correlated with tumor differentiation grade, microvascular invasion status, and molecular phenotypes (e.g., high Ki-67 expression and phosphatidylinositol proteoglycan 3 targeting). Furthermore, MRE's quantitative assessment of tumor hardness can provide objective support for prognostic stratification by accurately predicting the likelihood of postoperative recurrence. The non-invasive, reproducible, and quantitative advantages of MRE, which are based on the invasive assessment of HCC, demonstrate its unique clinical value. Multidimensional information in support of conventional imaging and molecular marker evaluation facilitates the early-stage diagnosis, personalized treatment, and dynamic monitoring of HCC.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 4","pages":"376-379"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783242","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":"[Research progress on poor response, resistance mechanisms, and influencing factors of immunotherapy for hepatocellular carcinoma].","authors":"M Huang, F N Zhang, H Gong, C C Liu, T T Zhao, N He","doi":"10.3760/cma.j.cn501113-20250902-00361","DOIUrl":"10.3760/cma.j.cn501113-20250902-00361","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Although immune checkpoint inhibitors offer hope for patients with advanced- stage HCC, the objective response rate remains only 15% to 30%, mainly due to primary or secondary drug resistance. This article systematically reviews the potential mechanisms and influencing factors of poor immunotherapy responses in HCC, aiming to provide theoretical reference for an in-depth understanding of primary non-response, secondary drug resistance, or immunotherapy resistance and the development of personalized treatment strategies.</p>","PeriodicalId":24006,"journal":{"name":"中华肝脏病杂志","volume":"34 4","pages":"392-399"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783212","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}