Hepatology Communications最新文献

{"title":"LIVE-SMART: A sequential, multiple assignment randomized trial to reduce falls in cirrhosis.","authors":"Elliot B Tapper, Samantha Nikirk, Donna M Evon, Sumeet Asrani, Patricia Bloom, James W Hynes, J Mark Alber, Anna Gill, Shivang Mehta, Ethan Weinberg, Neil B Alexander, Katie Althuis, Alise Hoelscher, Lili Zhao, Xi Chen, Alex Burdzy, Marina Serper","doi":"10.1097/HC9.0000000000000626","DOIUrl":"10.1097/HC9.0000000000000626","url":null,"abstract":"<p><strong>Introduction: </strong>Falls are a major threat to the well-being of patients with cirrhosis. We are performing a clinical trial to determine whether lactulose, TeleTai-Chi, or their combination will reduce falls in HE and improve health-related quality of life (HRQOL) among patients with cirrhosis.</p><p><strong>Methods and analysis: </strong>Patients with cirrhosis and portal hypertension without HE will be enrolled in 3 US states and followed participants for 24 weeks. In stage 1 (12 wk), participants will be randomized to receive either lactulose therapy or enhanced usual care. In stage 2 (12 wk), participants will be randomized to either TeleTai-Chi or usual care. The primary outcome is a hierarchical composite: Injurious falls, noninjurious falls, incident HE, and death/transplantation. Secondary outcomes include cognitive function, days-alive and out-of-hospital, and HRQOL. After completion of the interventions, participants will be followed for 48 weeks for health and financial outcomes.</p><p><strong>Ethics and dissemination: </strong>Our study has a central institutional review board with individual site IRB review. Dissemination includes the publication of study findings and patient-focused educational webinars.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 3","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143448641","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":"C/EBPβ transcription factor promotes alcohol-induced liver fibrosis in males via HDL remodeling.","authors":"Michael Schonfeld, Kruti Nataraj, Steven Weinman, Irina Tikhanovich","doi":"10.1097/HC9.0000000000000645","DOIUrl":"10.1097/HC9.0000000000000645","url":null,"abstract":"<p><strong>Background: </strong>Alcohol-associated liver disease (ALD) is the main cause of alcohol-associated mortality. However, the mechanism of ALD development is poorly understood. Epigenetic changes are thought to play an important role in ALD. We aimed to define the epigenetic changes induced by alcohol and predict drivers of these changes.</p><p><strong>Methods: </strong>Mice were fed high-fat diet with or without 20% of alcohol in the drinking water for 20 weeks (WDA model). scATAC-seq data set was analyzed using Signac R package. To test the role of C/EBPβ, Cebpb-floxed mice were treated with AAV8-TBG-Cre or AAV8-control.</p><p><strong>Results: </strong>We analyzed differentially accessible regions in livers from control and alcohol-fed mice and found that activity of C/EBPβ transcription factor was associated with alcohol-induced epigenetic changes in hepatocytes. C/EBPβ protein levels were significantly upregulated in multiple models of ALD and human ALD samples. Using hepatocyte-specific Cebpb knockout mice we found that Cebpb loss protected male mice from alcohol-induced fibrosis development. We found no protection in female mice, suggesting that this mechanism is specific to male ALD. In vitro studies suggested that the protective effect of Cebpb loss was mediated by altered hepatocyte-macrophage cross talk. Cebpb knockout in hepatocytes reduced a profibrotic and promoted a pro-resolving phenotype in macrophages, thus modulating ALD development. We further identified the mediators of the cross talk. Cebpb knockout altered the expression of several HDL protein components, increasing APOA1 and apolipoprotein M and reducing apolipoprotein E and SAA levels in male mice. HDL secreted by Cebpb knockout hepatocytes was sufficient to confer anti-inflammatory and antifibrotic changes to macrophages.</p><p><strong>Conclusions: </strong>Taken together, alcohol-induced C/EBPβ activation is a key driver of ALD fibrosis in males via C/EBPβ-dependent HDL remodeling.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 3","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143448360","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":"The impact of integrated care on clinical outcomes in patients with alcohol-associated liver disease: Early outcomes from a multidisciplinary clinic.","authors":"Shreya Sengupta, Akhil Anand, Qijun Yang, Meghan Reagan, Mariah Husted, Austin Minnick, Laura E Nagy, Srinivasan Dasarathy, Omar T Sims, Jessica L Mellinger","doi":"10.1097/HC9.0000000000000603","DOIUrl":"10.1097/HC9.0000000000000603","url":null,"abstract":"<p><strong>Background: </strong>We analyzed early outcomes regarding the impact of our integrated alcohol-associated liver disease (ALD) clinic on patients with ALD and alcohol use.</p><p><strong>Methods: </strong>We conducted a retrospective study of patients with ALD who were evaluated in our integrated clinic from May 1, 2022, to December 31, 2023. Primary outcomes included differences in baseline clinical/demographic data between patients who accepted versus declined an appointment and changes in the severity of ALD, alcohol consumption, functional status, hospital utilization, and remission in alcohol use disorder for evaluated patients.</p><p><strong>Results: </strong>Patients who declined appointments (n=66) had higher median no-show rates (15.0 [8.0,30.0] vs. 8.5 [3.25,15.0], p<0.001), social vulnerability index (0.53 [0.26,0.79] vs. 0.38 [0.17,0.63], p=0.033), and proportions of cirrhosis (78.8% vs. 59.8%, p=0.017) versus evaluated patients. Comparison of baseline to first follow-up visit for evaluated patients (n=102) demonstrated significant reductions in median AST (59.5 [41.75, 89] vs. 44.5 [33.5, 56.25], p<0.001), alanine-aminotransferase (33.5 [20,45.25] vs. 26.5 [18.75,33.0], p=0.017), total bilirubin (1.6 [0.7,3.3] vs. 1 [0.5,1.9], p=0.001), phosphatidylethanol (263 [35, 784] vs. 0 [0, 163], p<0.001), MELD-3.0 and Sodium scores for patients with alcohol-associated hepatitis and cirrhosis (16 [11, 18.75] vs. 12 [9, 14], p<0.001), 14 [9.25, 17.75] vs. 11 [8.5, 14], p<0.001), and Child-Turcotte-Pugh scores for patients with cirrhosis (9 [6, 10.5] vs. 7 [6, 9], p<0.001). The proportion of patients with active-severe alcohol use disorder significantly decreased (85.2% vs. 51.9%, p<0.001). Additionally, patients had significant reductions in emergency department utilization (incidence rate ratio of 0.64 emergency department visits/month (p=0.002) and 0.71 hospital admissions/month (p=0.025). However, after considering the false discovery rate, the reduction in hospitalization admissions/month was not statistically significant (False Discovery Rate adjusted p=0.056).</p><p><strong>Conclusions: </strong>Our integrated approach led to reductions in liver injury, degree of liver decompensation, alcohol use, and ED utilization, and remission in AUD in a population of both non-transplant ALD and post-transplant patients.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11810017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382328","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":"Loss of mitochondrial amidoxime-reducing component 1 (mARC1) prevents disease progression by reducing fibrosis in multiple mouse models of chronic liver disease.","authors":"Erin S Coyne, Yilin Nie, Darwin Lee, Sentibel Pandovski, Tiffany Yang, Heather Zhou, Thomas W Rosahl, Ester Carballo-Jane, Desiree Abdurrachim, Yongqi Zhou, Christopher Hendra, Asad Abu Bakar Ali, Stacey Meyers, Wendy Blumenschein, Brendan Gongol, Yang Liu, Yingjiang Zhou, Saswata Talukdar","doi":"10.1097/HC9.0000000000000637","DOIUrl":"10.1097/HC9.0000000000000637","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease is a prevalent disease that affects nearly one-third of the global population. Recent genome-wide association studies revealed that a common missense variant in the gene encoding mitochondrial amidoxime reducing component 1 (mARC1) is associated with protection from metabolic dysfunction-associated steatotic liver disease, all-cause cirrhosis, and liver-related mortality suggesting a role for mARC1 in liver pathophysiology; however, little is known about its function in the liver. In this study, we aimed to evaluate the impact of mARC1 hepatoprotective variants on protein function, the effect of loss of mARC1 on cellular lipotoxic stress response, and the effect of global or hepatocyte-specific loss of mARC1 in various mouse models of metabolic dysfunction-associated steatohepatitis and liver fibrosis.</p><p><strong>Methods and results: </strong>Expression and characterization of mARC1 hepatoprotective variants in cells and mouse liver revealed that the mARC1 p.A165T exhibited lower protein levels but maintained its mitochondrial localization. In cells, the knockdown of mARC1 improved cellular bioenergetics and decreased mitochondrial superoxide production in response to lipotoxic stress. Global genetic deletion and hepatocyte-specific knockdown of mARC1 in mice significantly reduced liver steatosis and fibrosis in multiple mouse models of metabolic dysfunction-associated steatohepatitis and liver fibrosis. Furthermore, RNA-seq analysis revealed that the pathways involved in extracellular matrix remodeling and collagen formation were downregulated in the liver, and the plasma lipidome was significantly altered in response to the loss of mARC1 in mice.</p><p><strong>Conclusions: </strong>Overall, we have demonstrated that loss of mARC1 alters hepatocyte response to lipotoxic stress and protects mice from diet-induced MASH and liver fibrosis consistent with findings from human genetics.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11809980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382327","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":"Distribution of culture-positive microorganisms varies with severity of liver disease in patients hospitalized with SBP.","authors":"Nadim Mahmud, Natalia Salinas Parra, Aaron L Hecht, David E Kaplan, Marina Serper","doi":"10.1097/HC9.0000000000000655","DOIUrl":"10.1097/HC9.0000000000000655","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peroxisome proliferator-activated receptor delta and liver diseases.","authors":"Tomoo Yamazaki, Edward E Cable, Bernd Schnabl","doi":"10.1097/HC9.0000000000000646","DOIUrl":"10.1097/HC9.0000000000000646","url":null,"abstract":"<p><p>Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors involved in transcriptional regulation and play an important role in many physiological and metabolic processes. Unlike PPAR-alpha and PPAR-gamma, PPAR-delta is ubiquitously expressed, and its activity is key to maintaining proper metabolic homeostasis within the liver. PPAR-delta not only regulates physiologic processes of lipid, glucose, and bile acid metabolism but also attenuates pathologic responses to alcohol metabolism, inflammation, fibrosis, and carcinogenesis, and is considered an important therapeutic target in liver diseases. Promising results have been reported in clinical trials for PPAR-delta agonists in liver disease, and the selective agonist seladelpar was recently conditionally approved in the United States as a new treatment option for primary biliary cholangitis. This review provides an overview of PPAR-delta's function and biology in the liver, examines its kinetics and therapeutic potential across different liver diseases, and discusses the current status of clinical trials involving its agonists.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH.","authors":"Gopanandan Parthasarathy, Nanditha Venkatesan, Guneet Singh Sidhu, Myeong Jun Song, Chieh-Yu Liao, Fanta Barrow, Amy Mauer, Tejasav Sehrawat, Yasuhiko Nakao, P Vineeth Daniel, Debanjali Dasgupta, Kevin Pavelko, Xavier S Revelo, Harmeet Malhi","doi":"10.1097/HC9.0000000000000613","DOIUrl":"10.1097/HC9.0000000000000613","url":null,"abstract":"<p><strong>Background: </strong>Immune cell-driven inflammation is a key mediator of metabolic dysfunction-associated steatohepatitis (MASH) progression. We have previously demonstrated that pharmacological sphingosine 1-phosphate (S1P) receptor modulation ameliorates MASH and is associated with attenuated accumulation of intrahepatic macrophage and T-cell subsets. Although S1P receptors are expressed on several immune cell types, given the prominent role of monocyte-derived recruited macrophages in the sterile inflammation of MASH, we hypothesized that deletion of S1P receptor 1 (S1P1) on myeloid cells may ameliorate MASH by reducing the accumulation of proinflammatory monocyte-derived macrophages in the liver.</p><p><strong>Methods: </strong>The LyzMCre approach was used to generate myeloid cell-specific knockout mice, termed S1pr1MKO. Littermate S1pr1loxp/loxp mice were used as wild-type controls. MASH was established by feeding mice a high-fat, -fructose, and -cholesterol (FFC) diet for 24 weeks, which led to the development of steatohepatitis and MASH-defining cardiometabolic risk factors. Liver injury and inflammation were determined by histological and gene expression analyses. Intrahepatic leukocyte populations were analyzed by mass cytometry and immunohistochemistry.</p><p><strong>Results: </strong>Histological examination demonstrated a reduction in liver inflammatory infiltrates and fibrosis in high-fat, -fructose, and -cholesterol-fed S1pr1MKO compared to wild-type. There was a corresponding reduction in alanine aminotransferase, a sensitive marker for liver injury. As determined by mass cytometry, a significant decrease in recruited macrophages was noted in the livers of high-fat, -fructose, and -cholesterol-fed S1pr1MKO mice compared to wild-type. Gene ontology pathway analysis revealed significant suppression of the peroxisome proliferator-activated receptor gamma and mitogen-activated protein kinase pathways in S1pr1MKO consistent with attenuated MASH in mice.</p><p><strong>Conclusions: </strong>Deletion of S1P1 in myeloid cells is sufficient to attenuate intrahepatic accumulation of monocyte-derived macrophages and ameliorate murine MASH.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Children with autoimmune hepatitis receiving standard-of-care therapy demonstrate long-term obesity and linear growth delay.","authors":"Or Steg Saban, Shannon M Vandriel, Syeda Aiman Fatima, Celine Bourdon, Amrita Mundh, Vicky L Ng, Simon C Ling, Robert H J Bandsma, Binita M Kamath","doi":"10.1097/HC9.0000000000000624","DOIUrl":"10.1097/HC9.0000000000000624","url":null,"abstract":"<p><strong>Background: </strong>Standard-of-care therapy in children with autoimmune hepatitis (AIH) includes induction with prednisone 1-2 mg/kg daily with gradual weaning of the dose. We aimed to test the hypothesis that children with AIH receiving standard-of-care treatment have altered growth trajectories.</p><p><strong>Methods: </strong>Children diagnosed with AIH between 1997 and 2023 at SickKids had serial growth measurements. Mixed effect models assessed the impact of time and daily steroid exposure on z-scores. Kaplan-Meier survival methods were used to estimate the cumulative incidence of new-onset growth impairments. A time-dependent Cox proportional hazards model was constructed to determine predictors for growth impairments.</p><p><strong>Results: </strong>Sixty-one children (66% females, median age at diagnosis 11.5 y) were included. BMIz showed a sharp increase, and HAZ declined significantly without returning to baseline. Each 1 mg/kg/d prednisone exposure increased BMIz gain in the first 6 months by 0.27 ([95% CI: 0.11, 0.42], p = 0.001), and decreased HAZ by -0.02 ([95% CI: -0.03, -0.01], p = 0.005). Children diagnosed before puberty exhibited a higher occurrence of excessive weight gain (72.2% vs. 49.3%; log-rank p < 0.01) and obesity (63% vs. 31.5%; log-rank p < 0.01) compared to those diagnosed during puberty. In a Cox proportional-hazards model, young age at diagnosis and daily prednisone dose >10 mg 6 months after diagnosis were predictors for linear growth delay.</p><p><strong>Conclusions: </strong>This study demonstrates that children with AIH receiving standard-of-care therapy demonstrate altered growth trajectories, long-term excess weight gain, obesity, and linear growth delay. Young age at diagnosis and >10 mg of daily prednisone at 6 months are predictors for linear growth delay. These data indicate the need to re-evaluate standard treatment algorithms for pediatric AIH in terms of steroid dosing and potential nonsteroid alternatives.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multidisciplinary clinic model enhances liver and metabolic health outcomes in adults with MASH.","authors":"Jonathan G Stine, David Bradley, Jennifer McCall-Hosenfeld, Victoria Motz-Patel, Justin Tondt, Sarah Batra, Britney Fitzgerald, Samantha Garcia, Breianna Hummer, Courtney Kindrew, Autumn Koppenhaver, Hannah Mohr, Nataliya Smith, Heather Tressler, Kyra VanKirk, Karen Krok, Ian Schreibman, Elizabeth Stonesifer, Kofi Clarke","doi":"10.1097/HC9.0000000000000649","DOIUrl":"10.1097/HC9.0000000000000649","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipokines regulate the development and progression of MASLD through organellar oxidative stress.","authors":"Ke Zhao, Heng Zhang, Wenyu Ding, Xiaoshuai Yu, Yanli Hou, Xihong Liu, Xinhua Li, Xiaolei Wang","doi":"10.1097/HC9.0000000000000639","DOIUrl":"10.1097/HC9.0000000000000639","url":null,"abstract":"<p><p>The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD), which is increasingly being recognized as a leading cause of chronic liver pathology globally, is increasing. The pathophysiological underpinnings of its progression, which is currently under active investigation, involve oxidative stress. Human adipose tissue, an integral endocrine organ, secretes an array of adipokines that are modulated by dietary patterns and lifestyle choices. These adipokines intricately orchestrate regulatory pathways that impact glucose and lipid metabolism, oxidative stress, and mitochondrial function, thereby influencing the evolution of hepatic steatosis and progression to metabolic dysfunction-associated steatohepatitis (MASH). This review examines recent data, underscoring the critical interplay of oxidative stress, reactive oxygen species, and redox signaling in adipokine-mediated mechanisms. The role of various adipokines in regulating the onset and progression of MASLD/MASH through mitochondrial dysfunction and endoplasmic reticulum stress and the underlying mechanisms are discussed. Due to the emerging correlation between adipokines and the development of MASLD positions, these adipokines are potential targets for the development of innovative therapeutic interventions for MASLD management. A comprehensive understanding of the pathogenesis of MASLD/MASH is instrumental for identifying therapies for MASH.</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/PMC11781772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058886","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}