Liver Research最新文献

{"title":"New drug therapies for metabolic dysfunction-associated steatohepatitis","authors":"John Y.L. Chiang","doi":"10.1016/j.livres.2025.01.001","DOIUrl":"10.1016/j.livres.2025.01.001","url":null,"abstract":"<div><div>The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has rapidly increased world-wide to 30%, with increasing of type 2 diabetes (T2D) and obesity in last two decades. The spectrum of MASLD covers from simple hepatic steatosis to the progressive metabolic dysfunction-associated steatohepatitis (MASH) with or without fibrosis, cirrhosis and hepatocellular carcinoma. The MASLD symptoms include dyslipidemia, hyperglycemia, insulin resistance and obesity, the liver manifestations of metabolic syndrome. Treatment option for MASH fibrosis is limited. Since the discovery of bile acids as the endogenous ligands of farnesoid X receptor (FXR) in early 1990, bile acid and FXR based-drug therapies have been developed and tested in clinical trials for cholestatic liver diseases and MASH fibrosis. However, many of these drugs have unwanted side-effects and moderate efficacy in improving fibrosis. The US Food and Drug Administration has not approved any of bile acid- and FXR-based drugs for MASH fibrosis. Drug therapies alternative to bile acid derivatives for MASH have been in clinical trials. Recently, resmetirom, a liver-specific- and thyroid hormone receptor beta-selective agonist has been approved for MASH fibrosis. Glucagon-like peptide-1 receptor agonists also are in clinical trials for MASH. This review covers recent development of novel drug therapies for MASH fibrosis, T2D and obesity.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 94-103"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanoparticle-based therapeutic strategies for chronic liver diseases: Advances and insights","authors":"Sathiyamoorthy Padmanaban ,&nbsp;Ji-Won Baek ,&nbsp;Sai Sahithya Chamarthy ,&nbsp;Saipriya Chandrasekaran ,&nbsp;Antony V Samrot ,&nbsp;Vijayakumar Gosu ,&nbsp;In-Kyu Park ,&nbsp;Kamalakannan Radhakrishnan ,&nbsp;Don-Kyu Kim","doi":"10.1016/j.livres.2025.04.002","DOIUrl":"10.1016/j.livres.2025.04.002","url":null,"abstract":"<div><div>The liver is pivotal in protein synthesis, glucose and lipid metabolism, and detoxification. However, the liver is susceptible to both acute and chronic disorders, with chronic conditions being fatal. Chronic liver diseases (CLDs), such as liver fibrosis, which usually represents the early manifestation of cirrhosis, primarily result from hepatitis B and C viruses infections, metabolic disorders, alcohol abuse, immune-mediated attacks, and cholestatic injury. The progression of liver fibrosis contributes to the development of cirrhosis, which can further lead to hepatocellular carcinoma, portal hypertension, hepatic decompensation, and hepatic encephalopathy. The extracellular matrix deposition over time leading the hepatocyte necrosis (cirrhosis) is the main structural feature of CLDs and may cause hepatic failure. Certain conditions, such as hepatitis and autoimmune diseases, may promote the rapid deterioration of liver function. Acute and chronic liver failure causes may vary, with early referral for liver transplantation improving the chance of recovery. The healthcare system need improvements to manage patients with non-alcoholic fatty liver disease and alcoholic fatty liver disease, as they have the potential to progress to cirrhosis. Both conditions involve the release of reactive oxygen species and damage-associated molecular patterns from cytokines, hepatic stellate cells, and hepatocyte autophagy, leading to prolonged inflammation. While various medications target fibrosis and liver damage, nanoparticle-based drug delivery systems offer additional promise by promoting faster liver regeneration. This review provides a comprehensive overview of the potential of nanoparticle systems as a future therapeutic approach for treating liver disorders.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 104-117"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell transcriptomic insights into endosulfan-induced liver injury: Key pathways and inflammatory responses","authors":"Pan Huang ,&nbsp;Yunmeng Bai ,&nbsp;Chaohua Zhou ,&nbsp;Xiaoru Zhong ,&nbsp;Ashok Iyaswamy ,&nbsp;Peng Chen ,&nbsp;Xu Wei ,&nbsp;Wei Zhang ,&nbsp;Chuanbin Yang ,&nbsp;Jigang Wang","doi":"10.1016/j.livres.2025.05.002","DOIUrl":"10.1016/j.livres.2025.05.002","url":null,"abstract":"<div><h3>Background and aims</h3><div>Environmental pollutants, particularly organochlorine insecticides like endosulfan (ENDO), are increasingly linked to liver toxicity and related diseases. Despite its widespread historical use, the mechanisms underlying ENDO-induced liver damage remain poorly understood. This study aims to elucidate the cellular and molecular mechanisms of ENDO-induced hepatotoxicity.</div></div><div><h3>Methods</h3><div>C57BL/6 mice were exposed to ENDO for two weeks. Single-cell RNA sequencing (scRNA-seq) was subsequently performed on mouse livers to explore ENDO-induced hepatotoxicity at the single-cell level. Differentially expressed genes (DEGs) across cell types and treatments were identified and then subjected to pathway enrichment to uncover key biological processes affected by ENDO. Transcription factor (TF) regulatory network, pseudotime trajectory, and cellular communication analysis were used to explore the molecular and cellular changes after ENDO exposure.</div></div><div><h3>Results</h3><div>ENDO not only caused direct hepatocyte injury but also activated hepatic stellate cells and lymphocytes, triggering inflammatory responses with upregulation of multiple key chemokines and cytotoxic genes. Additionally, ENDO exposure led to the recruitment and activation of myeloid cells, contributing to the inflammatory milieu. An increase in intercellular communication and changes to the hepatic microenvironment, especially the interaction between activated hepatic stellate cells and CD8⁺ T cells were observed, further implicating these processes in ENDO-induced liver damage.</div></div><div><h3>Conclusions</h3><div>This study provides new insights into the cellular and molecular mechanisms underlying liver injury induced by organochlorine insecticides like ENDO. Key genes and pathways involved in ENDO-associated liver toxicity have been identified at a single-cell resolution. These findings suggest that altered cellular communications and inflammatory responses may play pivotal roles in the pathogenesis of ENDO-induced liver injury.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 144-156"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A simplified and reproducible ex vivo model of cold and ischemia-reperfusion injury","authors":"Lele Zhang ,&nbsp;Mingjie Ding ,&nbsp;Ying Zhu ,&nbsp;Zhiping Yan ,&nbsp;Wenzhi Guo","doi":"10.1016/j.livres.2025.04.005","DOIUrl":"10.1016/j.livres.2025.04.005","url":null,"abstract":"<div><div>Both cold stress and ischemia-reperfusion injury significantly contribute to poor prognosis after liver transplantation (LT). However, limited animal models incorporating both stimuli hinder the advancement of transplant-related research. Here, a simplified and reproducible isolated perfused liver model is established to simulate the stresses experienced by livers maximally during transplantation. We provide a detailed protocol for a straightforward technique that requires 20–30 min for harvesting, 24–48 h for static cold storage (SCS), and 2 h for normothermic machine perfusion (NMP) to induce LT-like stresses in the liver. Hepatic injury from SCS and NMP (LT-like stresses) is evaluated using three types of parameters. The pH values and hepatic enzyme levels of cold preservation solutions and perfusate serve as dynamic indicators of hepatic injury. Bile production and portal venous resistance directly reflect liver function, whereas pathological analysis visually illustrates the location and extent of injury. This animal model eliminates the influence of hemodynamic and immune factors, yielding highly reproducible results, and is strongly recommended as a standardized animal model for inducing LT-like stresses.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 178-185"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"National Protect Liver Day 2025 in China: Integrating Traditional Chinese Medicine and Western Medicine to Reverse Liver Cirrhosis","authors":"Cuicui Shi,&nbsp;Jiangao Fan","doi":"10.1016/j.livres.2025.03.002","DOIUrl":"10.1016/j.livres.2025.03.002","url":null,"abstract":"","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 186-188"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-coding RNAs in alcohol-associated liver disease","authors":"Ge Zeng ,&nbsp;Hui Gao ,&nbsp;Yanchao Jiang ,&nbsp;Nazmul Huda ,&nbsp;Themis Thoudam ,&nbsp;Zhihong Yang ,&nbsp;Jing Ma ,&nbsp;Jian Sun ,&nbsp;Suthat Liangpunsakul","doi":"10.1016/j.livres.2025.04.007","DOIUrl":"10.1016/j.livres.2025.04.007","url":null,"abstract":"<div><div>Non-coding RNAs (ncRNAs), encompassing microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have emerged as critical regulators of gene expression and cellular function. In alcohol-associated liver disease (ALD), chronic alcohol consumption disrupts the expression and function of ncRNAs in the liver and circulation, contributing to the disease's pathogenesis and progression. Dysregulated ncRNAs influence key pathways involved in hepatocyte injury, lipid metabolism, inflammation, and hepatic stellate cell (HSC) activation, thereby exacerbating steatosis, inflammation, and fibrosis. Furthermore, extracellular vesicles play a pivotal role in mediating ncRNA-driven intercellular communication, amplifying liver damage and fibrosis. This review provides a comprehensive overview of the multifaceted roles of ncRNAs in ALD, with a focus on their mechanistic contributions to disease development and progression. Additionally, we discuss the potential of ncRNAs as diagnostic biomarkers and therapeutic targets, emphasizing their translational relevance in addressing the burden of ALD.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 81-93"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem cell-based therapeutic strategies for liver aging","authors":"Huan Niu ,&nbsp;Yan-Nan Wang ,&nbsp;Yu Ding ,&nbsp;Yu-Qing Lin ,&nbsp;Jian Qin ,&nbsp;Jian-Cheng Wang","doi":"10.1016/j.livres.2025.04.003","DOIUrl":"10.1016/j.livres.2025.04.003","url":null,"abstract":"<div><div>Aging is characterized by a gradual deterioration of the physiological integrity of cells, tissues, and organs, resulting in a decrease in the body’s physiological functions and an acceleration of the onset of age-related diseases, ultimately leading to death. The aging of the liver, which is a critical metabolic organ, is closely linked to various chronic liver diseases, such as hepatitis, liver fibrosis, and cirrhosis, and it exacerbates their prognosis and is a primary risk factor for their development at all stages. Therefore, a comprehensive understanding of the causes, mechanisms, and potential therapeutic targets associated with liver aging holds significant clinical importance for delaying or potentially reversing liver aging and for treating chronic liver diseases. Stem cells, which are potential anti-aging agents, present a promising and effective alternative for managing liver aging. In this review, we systematically assess the driving factors, characteristics, and underlying mechanisms of liver aging. We then discuss the current status of the use of stem cells to mitigate liver senescence and address related liver diseases. The review reveals that a stem cell-based approach represents a promising therapeutic strategy for combating liver aging and associated diseases.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 118-131"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rhizoma Atractylodis Macrocephalae reduces HFD-induced MAFLD in mice through activated AMPK-mediated inhibition of fatty acid synthesis","authors":"Ke Zheng ,&nbsp;Ruishuo Zhang ,&nbsp;Yijing Xin ,&nbsp;Yuge Zhou ,&nbsp;Jiacheng Lin ,&nbsp;Weifan Huang ,&nbsp;Fang Wang ,&nbsp;Liu Yang ,&nbsp;Xuehua Sun ,&nbsp;Xiaoni Kong","doi":"10.1016/j.livres.2025.04.004","DOIUrl":"10.1016/j.livres.2025.04.004","url":null,"abstract":"<div><h3>Background and aims</h3><div>Metabolic dysfunction-associated fatty liver disease (MAFLD) is a common chronic condition that can lead to cancer due to its complex pathogenesis. Therapeutic agents targeting AMP-activated protein kinase (AMPK) activation have been suggested as potential treatments for metabolic disorders such as metabolic dysfunction-associated steatohepatitis (MASH). Rhizoma Atractylodis Macrocephalae (RAM) has been clinically used to treat obesity-related health problems, but its therapeutic effects on MAFLD and the underlying mechanism remain unclear. Therefore, this study was conducted to evaluate the function and underlying mechanism of RAM in the treatment of MAFLD.</div></div><div><h3>Methods</h3><div>The effect of RAM decoction on MAFLD was evaluated using a high-fat diet (HFD)-induced MAFLD mouse model. <em>In vitro</em> studies were conducted using a palmitic acid/oleic acid-induced lipid accumulation model in the alpha mouse liver 12 cells and RAM-containing serum. The underlying mechanisms were elucidated through a combination of network pharmacology analysis, immunohistochemistry, western blotting, and polymerase chain reaction analysis.</div></div><div><h3>Results</h3><div>Administration of RAM decoction significantly reduced body weight gain in MAFLD mice without changing food intake. The weights of the liver and inguinal adipose tissues were also reduced after RAM treatment. Additionally, RAM administration decreased serum levels of alanine aminotransferase, aspartate transaminase, total cholesterol, triglyceride, low-density lipoprotein cholesterol, and glucose, while reducing lipid droplet accumulation in the liver tissues of MAFLD mice. The underlying mechanisms included the activation of the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC), and inhibition of the expression of sterol regulatory element binding protein 1 (SREBP1). However, RAM did not alter the protein expression levels of peroxisome proliferator-activated receptor α and carnitine palmitoyltransferase-1α. Furthermore, the RAM-induced upregulation of phosphorylated AMPK, phosphorylated ACC, and SREBP1 expression, as well as the downregulation of fatty acid synthase expression, were reversed by using an AMPK inhibitor.</div></div><div><h3>Conclusions</h3><div>Through a combination of network pharmacology and experimental validation, we demonstrated that RAM may exert therapeutic effects on MAFLD by inhibiting lipid synthesis and activating phosphorylated AMPK pathways.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 157-168"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-PD-1 synergizes with RFA to suppress abscopal tumors and induce durable memory against recurrence in HCC","authors":"Kai Lei ,&nbsp;Shuang Li ,&nbsp;Jiale Chen ,&nbsp;Zebin Chen ,&nbsp;Fang Wang ,&nbsp;Xuezhen Zeng","doi":"10.1016/j.livres.2025.05.003","DOIUrl":"10.1016/j.livres.2025.05.003","url":null,"abstract":"<div><h3>Background and aims</h3><div>Radiofrequency ablation (RFA) is the first-line treatment for early-stage hepatocellular carcinoma (HCC). However, recurrence after curative RFA remains a significant challenge for HCC patients. Although RFA induces an immune response, the anti-tumor effect is often limited by the immunosuppressive tumor microenvironment. Enhancing anti-tumor immunity is essential to improve treatment efficacy and prevent recurrence. In this study, we explore the efficacy and underlying mechanisms of the combination of RFA and anti-PD-1 in suppressing abscopal and recurrent tumors.</div></div><div><h3>Methods</h3><div>We established a bilateral subcutaneous HCC mouse model and performed complete RFA on the right-flank tumor. Anti-PD-1 or anti-IgG was administered post-RFA. Tumor growth, immune cell profiles, and molecular pathways were assessed using flow cytometry, immunohistochemistry staining, RNA-sequencing, and Western blot. Chemokines released by the tumor were detected by ELISA. An <em>in vivo</em> tumor rechallenge experiment was performed after a complete tumor regression to evaluate the immune memory induced by the RFA+anti-PD-1 treatment.</div></div><div><h3>Results</h3><div>RFA combined with anti-PD-1 significantly suppressed abscopal tumor growth and prolonged survival. Compared with RFA monotherapy, the infiltration of CD8⁺T cells and dendritic cells was significantly increased in the combined treatment group, while PMN-MDSCs were markedly reduced. Mechanistically, the chemokine signaling pathway and JAK-STAT signaling pathway were activated in the tumor of the RFA+anti-PD-1 group with upregulation of CXCL10 to recruit CD8⁺T cells. In addition, the combination therapy induced durable immune memory that inhibited rechallenge tumor outgrowth.</div></div><div><h3>Conclusions</h3><div>Our study discovered that RFA combined with anti-PD-1 induced anti-tumor immunity to inhibit abscopal tumors and durable immune memory to prevent recurrence, suggesting RFA+anti-PD-1 as a potential therapeutic strategy for multifocal HCC and preventing recurrence.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 132-143"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into the coexistence of Wilson’s disease and chronic hepatitis B: A retrospective propensity score matched study for improving clinical practice","authors":"Jiahui Pang ,&nbsp;Shuru Chen ,&nbsp;Yingfu Zeng,&nbsp;Yutian Chong,&nbsp;Weiqiang Gan,&nbsp;Xinhua Li","doi":"10.1016/j.livres.2024.12.003","DOIUrl":"10.1016/j.livres.2024.12.003","url":null,"abstract":"<div><h3>Background and aims</h3><div>Early and accurate diagnosis of the coexistence of Wilson’s disease (WD) and chronic hepatitis B (CHB) presents a significant challenge for clinicians. The objective of this study was to retrospectively analyse the characteristics of such patients to improve clinical practice and provide a reference for clinical management.</div></div><div><h3>Methods</h3><div>From January 2011 to December 2022, 35 patients with concurrent CHB and WD (CHB + WD group) were identified. A total of 127 patients with CHB (CHB group) and 168 patients with WD (WD group) were included in the control group between January 2016 and December 2021. Propensity score matching (PSM) was performed to balance the baseline values between groups. The Kaplan–Meier (K–M) survival analysis and log-rank test were performed to compare the prognoses.</div></div><div><h3>Results</h3><div>In the cohort of 35 patients with concurrent CHB and WD, 74.3% of patients (26 patients) faced a substantial delay of up to 10 years (range: 0–40 years) in WD diagnosis following their CHB diagnosis. Twenty-three (65.7%) patients had cirrhosis at the time of WD diagnosis, and 26 (74.3%) patients experienced liver failure. The levels of serum copper and uric acid were lower in patients in the CHB + WD group than in those in the CHB group. Patients in the CHB + WD group presented higher alanine transaminase and total bile acid levels compared to those in the WD group. K–M survival analysis indicated that patients with CHB and WD had poorer outcomes than those with CHB alone; however, the outcomes were similar to those of individuals with WD alone. The optimal cut-point of serum ceruloplasmin (CP) in identifying WD in CHB patients was 0.10 g/L before PSM and after PSM.</div></div><div><h3>Conclusions</h3><div>The present study emphasizes the importance of clinicians being vigilant for concurrent CHB and WD diagnoses, as delays in WD diagnosis may adversely affect patient outcomes. CHB patients with serum CP below 0.10 g/L are highly recommended to screen for WD.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 2","pages":"Pages 169-177"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144331291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}