Liver Research最新文献

{"title":"Nicotinic acid protects against hepatic ischemia-reperfusion injury via suppressing mitochondrial damage-induced ferroptosis","authors":"Qian Zeng ,&nbsp;Yina Sun ,&nbsp;Mengzhen Lei ,&nbsp;Zihan Liu ,&nbsp;Xijing Yan ,&nbsp;Rong Li ,&nbsp;Jun Zheng ,&nbsp;Jiandong Zha ,&nbsp;Lijun Zhang ,&nbsp;Xiaoling Guan ,&nbsp;Jia Yao","doi":"10.1016/j.livres.2025.11.001","DOIUrl":"10.1016/j.livres.2025.11.001","url":null,"abstract":"<div><h3>Background and aims</h3><div>Hepatic ischemia-reperfusion injury (HIRI) is a major contributor to liver dysfunction and failure, particularly in the context of liver transplantation. Its pathogenesis is primarily driven by ferroptosis, oxidative stress, and mitochondrial dysfunction. Given the interplay among these mechanisms through redox imbalance and disrupted energy metabolism, nicotinic acid (NA)—recognized for its antioxidative and metabolic regulatory properties—emerges as a promising therapeutic candidate. This study aims to investigate the protective effects of NA on HIRI and elucidate its underlying mechanisms.</div></div><div><h3>Methods</h3><div>An HIRI model in mice and a hypoxia/reoxygenation (H/R) model in primary hepatocytes were established to evaluate the effects of NA treatment on oxidative stress. NA was administered prior to model induction. <em>N</em>-acetylcysteine (NAC) was used as a comparator. Comprehensive assessments of ferroptosis, oxidative stress, mitophagy, and mitochondrial biogenesis markers were conducted using Western blotting, immunohistochemistry, immunofluorescence, and biochemical assays.</div></div><div><h3>Results</h3><div>NA pretreatment reduced serum alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase (LDH) levels, suppressed inflammation by decreasing neutrophil infiltration and macrophage activation, and mitigated oxidative stress by lowering reactive oxygen species (ROS) and malondialdehyde (MDA) levels. It enhanced antioxidant defenses, inhibited ferroptosis, and improved mitochondrial health through increased mitophagy, mitochondrial biogenesis, and mitochondrial permeability transition pore (mPTP) stabilization, leading to enhanced ATP production and mitochondrial function in HIRI.</div></div><div><h3>Conclusions</h3><div>NA improves mitochondrial function by promoting mitophagy and mitochondrial biogenesis, which reduces ferroptosis and oxidative stress, thereby alleviating HIRI.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 324-337"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802091","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":"Therapeutic potential of miRNA-26a-encapsulated nanoparticles against hepatocellular carcinoma in a murine model","authors":"Marwa Hassan ,&nbsp;Inés Fernández-Piñeiro ,&nbsp;Iker Badiola ,&nbsp;Mohamed Elzallat ,&nbsp;Alejandro Sánchez ,&nbsp;Tarek Aboushousha ,&nbsp;Ehab Hafiz ,&nbsp;Eman El-Ahwany","doi":"10.1016/j.livres.2025.10.002","DOIUrl":"10.1016/j.livres.2025.10.002","url":null,"abstract":"<div><h3>Background and aims</h3><div>Hepatocellular carcinoma (HCC) treatment options are limited due to the lack of effective curative therapies, and conventional chemotherapy has often demonstrated limited effectiveness and may be associated with significant toxicity. Therefore, innovative therapeutics for HCC are urgently needed. Here, we aimed to evaluate the effectiveness of microRNA (miRNA)-26a-encapsulated nanoparticles in HCC treatment.</div></div><div><h3>Methods</h3><div>Span-Oleylamine-chondroitin sulfate were prepared and eighty male BALB/c mice were divided into four groups: (i) negative control group (saline injection), (ii) HCC group (intraperitoneal injection of diethylnitrosamine (DEN), at 50 mg/kg/week for 18 weeks), (iii) miRNA-26a-treated HCC group (intrahepatical injection of 100 nmol free miRNA-26a once weekly for four weeks), and (iv) miRNA-26a-loaded nanoparticles-treated HCC group (intrahepatic injection of miRNA-26a-loaded nanoparticles once weekly for 4 weeks, starting from Week 14 of DEN induction). Then, all mice were subjected to biochemical, genetic, histopathological, and immunohistochemical examinations.</div></div><div><h3>Results</h3><div>The HCC group showed elevated serum levels of alpha-fetoprotein (AFP), des-gamma-carboxy prothrombin (DCP), vascular endothelial growth factor (VEGF), and tumor necrosis factor-alpha (TNF-alpha), along with upregulated hepatic expression of <em>P70S6K</em>, <em>transforming growth factor-beta</em>, <em>DNA methyltransferase 3 beta</em> (<em>DNMT3b</em>), and <em>Caspase-3</em> genes, as well as HepPar 1, Ki67, cyclin D1, and arginase 1 proteins (all <em>P</em> &lt; 0.001). miRNA-26a treatment attenuated these changes; moreover, the miRNA-26a-encapsulated nanoparticles caused a more dramatic decrease of these markers, resulting in almost complete restoration of the normal hepatic architecture.</div></div><div><h3>Conclusions</h3><div>Administration of miRNA-26a-encapsulated nanoparticles induced nearly total regression of HCC, suppression of cancer cell growth and angiogenesis, and induction of tumor necrosis. This study demonstrates the therapeutic efficacy of restoring the imbalanced expression of miRNA in the liver. Therefore, the clinical translation of this miRNA-based strategy warrants further investigation.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 338-350"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802092","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":"Sex differences in hepatic enzymes and transporters involved in pharmacokinetics","authors":"Mehak Behal,&nbsp;Zachary McCalla,&nbsp;Xinwen Wang","doi":"10.1016/j.livres.2025.10.003","DOIUrl":"10.1016/j.livres.2025.10.003","url":null,"abstract":"<div><div>Females experience adverse drug reactions at approximately twice the rate of males, contributing to drug-related morbidity and mortality in the United States. This disparity has been strongly associated with sex-based differences in pharmacokinetics. Hepatic drug-metabolizing enzymes and transporters, key regulators of pharmacokinetics, exhibit notable sex-based differences in expression and/or activity. However, findings on the sex-specific impacts of these enzymes and transporters are often scattered, highlighting the need for a comprehensive and up-to-date overview of knowledge in this area. This review compiles and analyzes existing data on sex differences in the expression and activity of clinically relevant hepatic drug-metabolizing enzymes and transporters across species, such as cytochrome P450s, UDP-glucuronosyltransferase, carboxylesterases, P-glycoprotein, breast cancer resistance protein, multidrug resistance-associated protein, organic anion-transporting polypeptides and organic cation transporters. It also summarizes how these differences influence clinical pharmacokinetics, adverse drug reactions, and drug dosing regimens. Furthermore, we explore potential underlying mechanisms, including the influence of sex hormones, sex chromosomes and lifestyle-related factors. Lastly, we discuss clinical implications and future directions in the field, highlighting the urgent need for more human-centered research to clarify the sex-specific impact on drug metabolism and transport in human. Such effort will support the development of sex-informed pharmacotherapy strategies that ultimately reduce adverse drug reactions and improve therapeutic outcomes for patients.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 253-272"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802138","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":"Metabolites involvement in the growth and spread of liver cancer","authors":"Anurag Kumar Gautam ,&nbsp;Vipin Kumar ,&nbsp;Archana Bharti Sonkar ,&nbsp;Amita Singh ,&nbsp;Deepankar Yadav ,&nbsp;Nitin Rajan ,&nbsp;Pranesh Kumar ,&nbsp;Sanjay Singh ,&nbsp;Sudipta Saha ,&nbsp;Vijayakumar Mahalingam Rajamanickam","doi":"10.1016/j.livres.2025.10.005","DOIUrl":"10.1016/j.livres.2025.10.005","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC), commonly known as primary liver cancer, is a leading cause of cancer-related mortality worldwide, primarily attributed to changing lifestyles and dietary habits. HCC arises from liver cirrhosis, hepatic fibrosis, or hepatitis B virus infection, and is caused by disruptions in protein and lipid metabolism. These metabolic alterations, recognized as a hallmark of cancer, are pivotal in the progression of chronic liver disease to HCC. Due to its asymptomatic nature in early stages, HCC is often diagnosed at advanced stages when treatment options are limited. Despite being a potentially curative option, liver transplantation remains hindered by high costs and donor scarcity, further compounded by suboptimal long-term success rates. This review examines the critical metabolites that play a part in developing HCC, focusing on their roles as possible biomarkers for disease progression and therapeutic targets. Additionally, the influence of the gut microbiome on HCC development is discussed, highlighting its interplay with metabolic pathways. Understanding the roles of metabolites and the gut microbiome in HCC progression underscores the importance of their potential use in early detection and the development of targeted therapies, offering new avenues for improving patient outcomes.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 286-297"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802140","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":"Spatiotemporal liver dynamics: How far can we take them in vitro?","authors":"Hanyang Liu","doi":"10.1016/j.livres.2025.11.002","DOIUrl":"10.1016/j.livres.2025.11.002","url":null,"abstract":"","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 359-361"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802088","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":"Resmetirom and beyond: A new era in MASLD therapeutics","authors":"Tejona Johnson-Moore,&nbsp;Dasia Simmons,&nbsp;Alvina Okafor,&nbsp;D'Era Washington,&nbsp;Padmamalini Baskaran","doi":"10.1016/j.livres.2025.10.004","DOIUrl":"10.1016/j.livres.2025.10.004","url":null,"abstract":"","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 362-364"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802089","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":"Corrigendum to “Metformin alleviates cholestasis-associated nephropathy through regulating oxidative stress and mitochondrial function” [Liver Res. 5 (2021) 171–180]","authors":"Mohammad Mehdi Ommati ,&nbsp;Hamidreza Mohammadi ,&nbsp;Khadijeh Mousavi ,&nbsp;Negar Azarpira ,&nbsp;Omid Farshad ,&nbsp;Reyhaneh Dehghani ,&nbsp;Asma Najibi ,&nbsp;Sedigheh Kamran ,&nbsp;Hossein Niknahad ,&nbsp;Reza Heidari","doi":"10.1016/j.livres.2025.12.001","DOIUrl":"10.1016/j.livres.2025.12.001","url":null,"abstract":"","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Page 365"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802090","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":"Targeting lactic acidosis in the tumor microenvironment: Enhancing TACE efficacy in hepatocellular carcinoma","authors":"Shuyi Hao ,&nbsp;Hong Yao ,&nbsp;Haojie Yu ,&nbsp;Lijun Wang ,&nbsp;Tingdong Yu ,&nbsp;Hongping Xia ,&nbsp;Yong Zha","doi":"10.1016/j.livres.2025.11.004","DOIUrl":"10.1016/j.livres.2025.11.004","url":null,"abstract":"<div><div>Lactic acidosis is a hallmark of the tumor microenvironment (TME) and a critical impediment to the efficacy of transarterial chemoembolization (TACE) in hepatocellular carcinoma (HCC). Incomplete embolization preserves viable tumor cells that amplify hypoxia-driven glycolysis, generating a lactic acid-rich milieu that drives treatment resistance, skews immune populations toward immunosuppressive phenotypes, and impairs cytotoxic T lymphocyte function. In this review, we elucidate the pathways through which lactic acidosis compromises TACE efficacy and propose novel strategies for its mitigation. We examine emerging approaches, including systemic or intra-arterial alkalization, targeted inhibition of lactate production and export, and calcium carbonate nanoparticles, and evaluate their respective merits and limitations. Finally, we propose a combination regimen of calcium carbonate nanoparticles, lactate-targeting agents, and TACE to achieve precise drug delivery, synergistic lactic acid depletion, and enhanced antitumor immunity. These integrated strategies have the potential to convert immunologically “cold” HCC lesions into “hot” ones, thereby improving TACE outcomes and disease control.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 273-285"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802139","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":"Cancer cachexia-related monocytic myeloid-derived suppressor cells impair T-cell negative selection and predict immune-related adverse events","authors":"Li Wei ,&nbsp;Ya-Qin Sun ,&nbsp;Jian-Hua Ren ,&nbsp;Ze-Xuan Huang ,&nbsp;Yuan Zhang ,&nbsp;Xiu-Qing Pang ,&nbsp;Xiao-Tong Lv ,&nbsp;Xiang-Yuan Wu ,&nbsp;Yan-Fang Xing ,&nbsp;Xing Li","doi":"10.1016/j.livres.2025.10.001","DOIUrl":"10.1016/j.livres.2025.10.001","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background and aims&lt;/h3&gt;&lt;div&gt;Cancer cachexia is prevalent in various cancers and is associated with chemotherapy toxicity. However, limited data exist on the relationship between cachexia and immune-related adverse events (irAEs). The aim of this study is to explore the correlation between cancer cachexia and irAEs and its possible mechanism.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;A murine model of orthotopic hepatocellular carcinoma (HCC) with cachexia was developed to evaluate the impact of T-cell infiltration into multiple tumor-free organs on the occurrence of irAEs. Single-cell RNA sequencing of thymic stromal cells was performed. Additionally, patients with advanced cancers receiving anti-programmed cell death protein 1/ligand 1 (PD-1/L1) antibody treatment were followed to investigate the relationship between cachexia and irAEs.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Inflammatory cell infiltration was observed in multiple tumor-free organs of cachexic HCC mice but not in non-cachexic controls. Immunofluorescence confirmed that the infiltrating cells included CD4&lt;sup&gt;+&lt;/sup&gt; and CD8&lt;sup&gt;+&lt;/sup&gt; T cells. Morphological assessment and hematoxylin–eosin staining revealed thymic atrophy in cachexic HCC mice. Single-cell RNA sequencing of thymic stromal cells showed a reduction in medullary thymic epithelial cells (mTECs) II and III in cachexic mice. Autoimmune regulator (Aire) downregulation was accompanied by decreased expression of tissue-restricted antigens in mTECs. T cells from cachexic HCC mice induced organ-specific inflammation and T-cell infiltration in multiple organs of tumor-free mice. Following anti-mouse PD-1 antibody treatment, the incidence of inflammation in multiple organs markedly increased in cachexic HCC mice and in tumor-free mice that had received T cells from the cachexic HCC mice. Flow cytometry and immunofluorescence analyses revealed enrichment of thymic monocytic myeloid-derived suppressor cells (M-MDSCs) in cachexic HCC mice. M-MDSCs infiltrated the thymus in cachexic mice with cancer, and they induced apoptosis of mTECs from tumor-free mice &lt;em&gt;in vitro&lt;/em&gt; via nitric oxide production. Transfer of M-MDSCs led to inflammatory cell infiltration in multiple organs and thymic involution in tumor-free mice without affecting body weight. Sixty-four patients with advanced cancer receiving anti-PD-1/L1 therapy were enrolled. Patients who developed irAEs had higher levels of circulating M-MDSCs than those who did not. Moreover, patients with cachexia (body mass index (BMI) &lt; 20 kg/m&lt;sup&gt;2&lt;/sup&gt; or ≥5% weight loss over the past 6 months) had elevated M-MDSC levels. Patients with both high M-MDSC levels and low BMI or weight loss ≥5% experienced more irAEs (hazard ratio: 2.333; 95% confidence interval: 1.231–4.423).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;M-MDSCs in cachexic mice induced mTEC apoptosis through nitric oxide production, impairing T-cell negative selection and promoting autoimmune T-cell infiltration in","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 298-312"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802141","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":"Comparative study of 3D MR elastography and intravoxel incoherent motion for the evaluation of hepatocellular carcinoma grade","authors":"Weimin Liu ,&nbsp;Sidong Xie ,&nbsp;Wenjie Tang ,&nbsp;Ka Zhang","doi":"10.1016/j.livres.2025.11.003","DOIUrl":"10.1016/j.livres.2025.11.003","url":null,"abstract":"<div><h3>Background and aims</h3><div>Noninvasive preoperative radiologic prediction of histologic grade—a key prognostic factor—is invaluable. We aim to compare the diagnostic values of 3D magnetic resonance elastography (MRE), intravoxel incoherent motion (IVIM), and conventional contrast-enhanced magnetic resonance imaging (cMRI) in predicting the histologic grade of hepatocellular carcinoma (HCC).</div></div><div><h3>Methods</h3><div>This institutional review board-approved retrospective study included patients who underwent MRI between December 2014 and October 2021. Sixty-eight patients with pathologically confirmed HCCs who underwent MRE, IVIM, and cMRI imaging were included in the analysis. Two radiologists measured HCC stiffness volumetrically and over a single slice, and also measured apparent diffusion coefficient (ADC), IVIM-derived parameters, and enhancement ratio (ER) on arterial phase images via cMRI. Student’s <em>t</em>-test or the Mann–Whitney <em>U</em> test was used for group comparisons. Receiver operating characteristic (ROC) curve analyses were performed to evaluate the diagnostic performance.</div></div><div><h3>Results</h3><div>Histologically, fifty-three (78%) patients had well-differentiated or moderately differentiated HCCs, and fifteen (22%) patients had poorly differentiated HCCs. Both the volumetric stiffness and single-ROI tumor stiffness were significantly elevated in the poorly differentiated HCC group (<em>P</em> &lt; 0.001, <em>P</em> = 0.001), and the volumetric stiffness was a better measurement of stiffness because it had a higher ROC curve value (0.816). However, the ADC, the true diffusion coefficient (D), the pseudodiffusion coefficient (D∗), the pseudodiffusion fraction (f), and ER during the arterial phases on cMRI were not significantly different between the two groups (<em>P</em> = 0.309, 0.187, 0.440, 0.350, and 0.714, respectively).</div></div><div><h3>Conclusions</h3><div>Stiffness measured with 3D MRE may be useful for noninvasively predicting HCC histologic grade, and the volumetric measuring method achieved the highest ROC curve value, outperforming single-ROI HCC stiffness, IVIM parameters, and arterial-phase ER on cMRI.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"9 4","pages":"Pages 351-358"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802136","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}