Hepatology Communications最新文献

{"title":"Hepatocyte Rho-associated kinase signaling is required for mice to survive experimental porphyria-associated liver injury.","authors":"Jessica M Herrera, Yun Weng, Tyler J Lieberthal, Marcus Paoletti, Tammy T Chang","doi":"10.1097/HC9.0000000000000636","DOIUrl":"10.1097/HC9.0000000000000636","url":null,"abstract":"<p><strong>Background: </strong>Rho-associated kinases 1 and 2 (ROCK1 and ROCK2) regulate critical cell functions, including actomyosin contractility, apoptosis, and proliferation. Some studies suggest that ROCK inhibition may serve as a treatment for liver fibrosis. More investigation is needed to understand the role of hepatocyte ROCK signaling in vivo, especially in the context of profibrotic liver injury.</p><p><strong>Methods: </strong>Rock1fl/fl, Rock2fl/fl, and Rock1fl/fl; Rock2fl/fl mice were given adeno-associated virus serotype 8 (AAV8)-thyroid hormone-binding globulin (TBG)-Cre to produce targeted gene deletion in hepatocytes, or given AAV8-TBG-Null to generate littermate controls (WT). Mice were then placed on a 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet to induce liver injury.</p><p><strong>Results: </strong>Upon DDC-induced liver injury, mice with hepatocyte-specific deletion of ROCK1 alone (R1 KO) or ROCK2 alone (R2 KO) demonstrated minimal differences compared to WT. In contrast, mice with hepatocyte-specific deletion of both ROCK1 and ROCK2 (DKO) showed pervasive early mortality, increased hepatocellular injury, and decreased hepatic function. DDC-injured DKO mice demonstrated markedly distorted liver histology characterized by large cavities in the parenchyma. RNA-seq analysis showed upregulation of cell death, inflammatory, and profibrotic pathways in DDC-injured DKO liver as compared to DDC-injured WT liver. Cdkn1a (gene encoding p21) was one of the most highly upregulated genes in the DKO liver in response to DDC-induced injury. Correspondingly, there was increased hepatocyte nuclear localization of p21 and expression of cleaved caspase-3 in DDC-injured DKO liver, consistent with the activation of p21-mediated caspase-3-dependent apoptotic cell death pathways. ROCK1/ROCK2-deficient primary hepatocytes demonstrated increased susceptibility to both caspase-3-mediated apoptosis and caspase-3-independent forms of cell death in a cell intrinsic manner.</p><p><strong>Conclusions: </strong>ROCK signaling plays a critical role in mediating hepatocyte cell survival pathways in response to liver injury.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HBV and HBsAg strongly reshape the phenotype, function, and metabolism of DCs according to patients' clinical stage.","authors":"Lucile Dumolard, Theophile Gerster, Florent Chuffart, Thomas Decaens, Marie-Noelle Hilleret, Sylvie Larrat, Philippe Saas, Evelyne Jouvin-Marche, David Durantel, Patrice N Marche, Zuzana Macek Jilkova, Caroline Aspord","doi":"10.1097/HC9.0000000000000625","DOIUrl":"10.1097/HC9.0000000000000625","url":null,"abstract":"<p><strong>Background: </strong>Hepatitis B is a liver infection caused by HBV. Infected individuals who fail to control the viral infection develop chronic hepatitis B and are at risk of developing life-threatening liver diseases, such as cirrhosis or liver cancer. Dendritic cells (DCs) play important roles in the immune response against HBV but are functionally impaired in patients with chronic hepatitis B. The underlying mechanisms involved in HBV-induced DC dysfunctions remain to be elucidated.</p><p><strong>Methods: </strong>We explored DC modulations by HBV and HBsAg by exposing blood-derived cDC1s, cDC2s, and plasmacytoid DCs from healthy donors to HBV or HBsAg and stimulating them with toll-like receptor ligand. Their phenotypic and functional features, as well as their metabolic profile, were analyzed through multiparametric flow cytometry and multiplex assays and further explored on patients' samples.</p><p><strong>Results: </strong>We found that HBV deeply reshaped the DC secretome in response to toll-like receptor ligand. Strikingly, we observed that HBV-exposed DCs secrete high levels of CX3CL1 (fractalkine), a chemokine responsible for attracting antiviral effectors to the site of infection. HBsAg exposure favored DC activation while drastically altering TRAIL expression in response to toll-like receptor ligand and increasing the secretion of cytokines/chemokines involved in immune tolerance. HBsAg further dampened the metabolism of DC subsets while driving metabolic switches. Notably, the relevance of the CX3CL1/CX3CR1 axis, TGF-β, and metabolic disturbances was demonstrated within intrahepatic DC subsets in patients according to disease stage.</p><p><strong>Conclusions: </strong>Our work brings new insights into the immunomodulation induced by HBV on DCs, which contribute to impaired antiviral responses and progression toward chronicity.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocyte-derived liver progenitor-like cells attenuate liver cirrhosis via induction of apoptosis in hepatic stellate cells.","authors":"Xu Zhou, Wen-Ming Liu, Han-Yong Sun, Yuan Peng, Ren-Jie Huang, Cai-Yang Chen, Hong-Dan Zhang, Shen-Ao Zhou, Hong-Ping Wu, Dan Tang, Wei-Jian Huang, Han Wu, Qi-Gen Li, Bo Zhai, Qiang Xia, Wei-Feng Yu, He-Xin Yan","doi":"10.1097/HC9.0000000000000614","DOIUrl":"10.1097/HC9.0000000000000614","url":null,"abstract":"<p><strong>Background: </strong>Cell therapy demonstrates promising potential as a substitute therapeutic approach for liver cirrhosis. We have developed a strategy to effectively expand murine and human hepatocyte-derived liver progenitor-like cells (HepLPCs) in vitro. The primary objective of the present study was to apply HepLPCs to the treatment of liver cirrhosis and to elucidate the underlying mechanisms responsible for their therapeutic efficacy.</p><p><strong>Methods: </strong>The effects of allogeneic or xenogeneic HepLPC transplantation were investigated in rat model of liver cirrhosis. Liver tissues were collected and subjected to immunostaining to assess changes in histology. In vitro experiments used HSCs to explore the antifibrotic properties of HepLPC-secretomes and their underlying molecular mechanisms. Additionally, proteomic analysis was conducted to characterize the protein composition of HepLPC-secretomes.</p><p><strong>Results: </strong>Transplantation of HepLPCs resulted in decreased active fibrogenesis and net fibrosis in cirrhosis models. Apoptosis of HSCs was observed in vivo after HepLPC treatment. HepLPC-secretomes exhibited potent inhibition of TGF-β1-induced HSC activation and promoted apoptosis through signal transducer and activator of transcription (STAT)1-mediated pathways in vitro. Furthermore, synergistic effects between amphiregulin and FGF19 within HepLPC-secretomes were identified, contributing to HSC apoptosis and exerting antifibrotic effects via activation of the janus kinase-STAT1 pathway.</p><p><strong>Conclusions: </strong>HepLPCs have the potential to ameliorate liver cirrhosis by inducing STAT1-dependent apoptosis in HSCs. Amphiregulin and FGF19 are key factors responsible for STAT1 activation, representing promising novel therapeutic targets for the treatment of liver cirrhosis.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-term costs of alcohol-associated hepatitis care in different clinical settings.","authors":"Chi Mai Nguyen, Jing Su, Yang Li, Ryan Healey, Shihui Jiang, Jiangqiong Li, Naga Chalasani, Samer Gawrieh, Suthat Liangpunsakul, Wanzhu Tu","doi":"10.1097/HC9.0000000000000634","DOIUrl":"10.1097/HC9.0000000000000634","url":null,"abstract":"<p><strong>Background: </strong>Alcohol-associated hepatitis (AH) leads to high rates of mortality and health care costs. Understanding the immediate costs after an AH diagnosis and identifying key cost factors is crucial for health care policies and clinical decisions.</p><p><strong>Objectives: </strong>This study quantifies medical costs within 30 days of an AH diagnosis across outpatient (OP), emergency department (ED), and inpatient (IP) settings. It also explores concurrent diagnoses and their effects on care costs.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study using deidentified data from Optum's Clinformatics Data Mart. The cohort included individuals aged 21 years and older diagnosed with AH from January 1, 2016, to September 30, 2023. Patients were categorized by care setting (OP, ED, or IP). Costs were calculated for the 30 days before and after AH diagnosis and adjusted to 2023-dollar values. Comorbidities were identified using Elixhauser comorbidity software, and multivariable linear regression models were used to analyze medical costs.</p><p><strong>Results: </strong>The cohort included 34,974 individuals diagnosed with AH: 8048 in OP (23%), 2736 in ED (7.8%), and 24,190 in IP (69.2%). Average spending in the 30 days prior to AH diagnosis was $7334 for OP, $5740 for ED, and $14,458 for IP. Following AH diagnosis, average costs rose to $8345 for OP, $20,990 for ED, and $88,655 for IP, reflecting increases of 14%, 266%, and 413%, respectively. Significant cost drivers in IP included comorbidities associated with moderate-to-severe liver disease, metabolic syndrome, liver transplant, and mortality during the 30-day follow-up period.</p><p><strong>Conclusions: </strong>Immediate costs following an AH diagnosis are substantial, particularly for IP care. Costs increase significantly with high-cost comorbidity clusters and among patients who die, underscoring the need for effective management of comorbidities in AH care.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygenic risk score in cirrhosis: Does the etiology matter?","authors":"Marta Alonso-Peña, Maria Teresa Arias Loste, Joaquin Cabezas, Paula Iruzubieta, Javier Crespo","doi":"10.1097/HC9.0000000000000541","DOIUrl":"10.1097/HC9.0000000000000541","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrogen peroxide damage to rat liver sinusoidal endothelial cells is prevented by n-acetyl-cysteine but not GSH.","authors":"Larissa D Kruse, Christopher Holte, Bartlomiej Zapotoczny, Eike C Struck, Jasmin Schürstedt, Wolfgang Hübner, Thomas Huser, Karolina Szafranska","doi":"10.1097/HC9.0000000000000617","DOIUrl":"10.1097/HC9.0000000000000617","url":null,"abstract":"<p><strong>Background: </strong>Reactive oxygen species (ROS) are prevalent in the liver during intoxication, infection, inflammation, and aging. Changes in liver sinusoidal endothelial cells (LSEC) are associated with various liver diseases.</p><p><strong>Methods: </strong>Isolated rat LSEC were studied under oxidative stress induced by H2O2 at different concentrations (0.5-1000 µM) and exposure times (10-120 min). LSEC functions were tested in a dose-dependent and time-dependent manner.</p><p><strong>Results: </strong>(1) Cell viability, reducing potential, and scavenging function decreased as H2O2 concentration and exposure time increased; (2) intracellular ROS levels rose with higher H2O2 concentrations; (3) fenestrations exhibited a dynamic response, initially closing but partially reopening at H2O2 concentrations above 100 µM after about 1 hour; (4) scavenging function was affected after just 10 minutes of exposure, with the impact being irreversible and primarily affecting degradation rather than receptor-mediated uptake; (5) the tubulin network was disrupted in high H2O2 concentration while the actin cytoskeleton appears to remain largely intact. Finally, we found that reducing agents and thiol donors such as n-acetyl cysteine and glutathione (GSH) could protect cells from ROS-induced damage but could not reverse existing damage as pretreatment with n-acetyl cysteine, but not GSH, reduced the negative effects of ROS exposure.</p><p><strong>Conclusions: </strong>The results suggest that LSEC does not store an excess amount of GSH but rather can readily produce it in the occurrence of oxidative stress conditions. Moreover, the observed thresholds in dose-dependent and time-dependent changes, as well as the treatments with n-acetyl cysteine/GSH, confirm the existence of a ROS-depleting system in LSEC.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply: Polygenic risk score in cirrhosis: Does the etiology matter?","authors":"Tae-Hwi Schwantes-An, Timothy R Morgan, Devanshi Seth","doi":"10.1097/HC9.0000000000000543","DOIUrl":"10.1097/HC9.0000000000000543","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Duodenal-jejunal bypass ameliorates MASLD in rats by regulating gut microbiota and bile acid metabolism through FXR pathways.","authors":"Mengting Ren, Yi Xia, Hanghai Pan, Xinxin Zhou, Mosang Yu, Feng Ji","doi":"10.1097/HC9.0000000000000615","DOIUrl":"10.1097/HC9.0000000000000615","url":null,"abstract":"<p><strong>Background: </strong>Although bariatric and metabolic surgical methods, including duodenal-jejunal bypass (DJB), were shown to improve metabolic dysfunction-associated steatotic liver disease (MASLD) in clinical trials and experimental rodent models, their underlying mechanisms remain unclear. The present study therefore evaluated the therapeutic effects and mechanisms of action of DJB in rats with MASLD.</p><p><strong>Methods: </strong>Rats with MASLD were randomly assigned to undergo DJB or sham surgery. Rats were orally administered a broad-spectrum antibiotic cocktail (Abx) or underwent fecal microbiota transplantation to assess the role of gut microbiota in DJB-induced improvement of MASLD. Gut microbiota were profiled by 16S rRNA gene sequencing and metagenomic sequencing, and bile acids (BAs) were analyzed by BA-targeted metabolomics.</p><p><strong>Results: </strong>DJB alleviated hepatic steatosis and insulin resistance in rats with diet-induced MASLD. Abx depletion of bacteria abrogated the ameliorating effects of DJB on MASLD. Fecal microbiota transplantation from rats that underwent DJB improved MASLD in high-fat diet-fed recipients by reshaping the gut microbiota, especially by significantly reducing the abundance of Clostridium. This, in turn, suppressed secondary BA biosynthesis and activated the hepatic BA receptor, farnesoid X receptor. Inhibition of farnesoid X receptor attenuated the ameliorative effects of post-DJB microbiota on MASLD.</p><p><strong>Conclusions: </strong>DJB ameliorates MASLD by regulating gut microbiota and BA metabolism through hepatic farnesoid X receptor pathways.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of clinical outcomes in patients with refractory ascites treated with either TIPS, tunneled peritoneal catheter, or ascites pump.","authors":"Sarah L Schütte, Anja Tiede, Jim B Mauz, Hannah Rieland, Martin Kabelitz, Robin Iker, Nicolas Richter, Bernhard Meyer, Benjamin Heidrich, Heiner Wedemeyer, Benjamin Maasoumy, Tammo L Tergast","doi":"10.1097/HC9.0000000000000620","DOIUrl":"10.1097/HC9.0000000000000620","url":null,"abstract":"<p><strong>Background: </strong>Refractory ascites (RA) remains a serious complication in patients with cirrhosis. Currently, the insertion of a TIPS is considered the standard of care in these patients. To achieve symptom control in those with TIPS contraindications, tunneled peritoneal catheters (PeCa) or ascites pumps were introduced. However, data comparing the available treatment options are scarce. This study aims to compare outcomes among patients with RA treated either with TIPS, PeCa, or ascites pump.</p><p><strong>Methods: </strong>All patients with RA and cirrhosis treated at Hannover Medical School between 2009 and 2023 were evaluated. Endpoints included mortality, acute kidney injury (AKI), hyponatremia, peritonitis, and rehospitalization rate. Propensity score matching was conducted to adjust for group differences.</p><p><strong>Results: </strong>First, 31 patients with ascites pump were compared to 62 patients with a PeCa after propensity score matching. There were no differences regarding mortality nor incidences of AKI, hyponatremia, or rehospitalization. However, incidences of peritonitis and explantation were lower in those with ascites pump (HR 0.32, 95% CI: 0.15-0.70, and HR 0.32, 95% CI: 0.14-0.71, respectively). Second, 35 ascites pump patients were matched with 70 individuals with TIPS. No differences regarding mortality or peritonitis incidence were observed. Ascites pump patients showed higher incidences of AKI (HR 4.55, 95% CI: 2.53-8.18) and hyponatremia (HR 4.13, 95% CI: 2.08-8.22). Last, 129 patients with TIPS were compared to 129 with PeCa. Mortality was comparable, while incidences of AKI (HR 5.01, 95% CI: 3.36-7.47), hyponatremia (HR 4.64, 95% CI: 3.03-7.12), and peritonitis (HR 2.19, 95% CI: 1.41-3.41) were higher in those with PeCa.</p><p><strong>Conclusions: </strong>While ascites pump was associated with lower incidences of device infections and explantations, TIPS was associated with the lowest incidence of clinical complications in patients with RA.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental exposures and the risk of hepatocellular carcinoma.","authors":"Divya Rayapati, Katherine A McGlynn, John D Groopman, Amy K Kim","doi":"10.1097/HC9.0000000000000627","DOIUrl":"10.1097/HC9.0000000000000627","url":null,"abstract":"<p><p>The global epidemiology of HCC is shifting due to changes in both established and emerging risk factors. This transformation is marked by an emerging prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes, alongside traditional risks such as viral hepatitis (HBV and HCV), and exposure to chemical agents like aflatoxin, alcohol, tobacco, and air pollution. This review examines how environmental exposures and evolving liver pathology, exacerbated by lifestyle and metabolic conditions, are contributing to the rising worldwide incidence of HCC. Effective prevention strategies must not only address traditional risk factors through vaccination and therapeutic measures but also confront metabolic and socioeconomic disparities through comprehensive public health efforts. As the burden of liver cancer continues to grow, particularly in resource-limited settings, an expansive and inclusive approach is vital for mitigating its impact across diverse populations.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}