Journal of Clinical and Translational Hepatology最新文献

{"title":"Unraveling the Role of the Wnt Pathway in Hepatocellular Carcinoma: From Molecular Mechanisms to Therapeutic Implications.","authors":"Zixin Liang, Shanshan Li, Zhiyu Wang, Junting Zhou, Ziyue Huang, Jiehan Li, Haolin Bao, Judy Wai Ping Yam, Yi Xu","doi":"10.14218/JCTH.2024.00401","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00401","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the deadliest malignant tumors in the world, and its incidence and mortality have increased year by year. HCC research has increasingly focused on understanding its pathogenesis and developing treatments.The Wnt signaling pathway, a complex and evolutionarily conserved signal transduction system, has been extensively studied in the genesis and treatment of several malignant tumors. Recent investigations suggest that the pathogenesis of HCC may be significantly influenced by dysregulated Wnt/β-catenin signaling. This article aimed to examine the pathway that controls Wnt signaling in HCC and its mechanisms. In addition, we highlighted the role of this pathway in HCC etiology and targeted treatment.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"315-326"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 Liver Graft Preservation Method on Longitudinal Gut Microbiome Changes Following Liver Transplant: A Proof-of-concept Study.","authors":"Gail A M Cresci, Qiang Liu, Naseer Sangwan, Darren Liu, David Grove, David Shapiro, Khaled Ali, Beatrice Cazzaniga, Luca Del Prete, Charles Miller, Koji Hashimoto, Cristiano Quintini","doi":"10.14218/JCTH.2024.00352","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00352","url":null,"abstract":"<p><strong>Background and aims: </strong>End-stage liver disease is associated with disruptions in gut microbiota composition and function, which may facilitate gut-to-liver bacterial translocation, impacting liver graft integrity and clinical outcomes following liver transplantation. This study aimed to assess the impact of two liver graft preservation methods on fecal microbiota and changes in fecal and breath organic acids following liver transplantation.</p><p><strong>Methods: </strong>This single-center, non-randomized prospective pilot study enrolled liver transplant patients whose grafts were preserved using either static cold storage or ex situ normothermic machine perfusion (NMP). Fresh stool and breath samples were collected immediately before surgery and at postoperative months 3, 6, and 12. Stool microbiota was profiled via 16S rRNA gene sequencing, stool short-chain fatty acids were measured using gas chromatography/-mass spectrometry, and breath volatile organic compounds (VOCs) were analyzed with selected-ion flow-tube mass spectrometry.</p><p><strong>Results: </strong>Both cohorts experienced a loss of microbiota diversity and dominance by single taxa. The NMP cohort demonstrated enrichment of several beneficial gut taxa, while the static cold storage cohort showed depletion of such taxa. Various gut bacteria were found to correlate with stool short-chain fatty acids (e.g., lactic acid, butyric acid) and several VOCs.</p><p><strong>Conclusions: </strong>Fecal microbiota alterations associated with end-stage liver disease do not fully normalize to a healthy control profile following liver transplantation. However, notable differences in microbiota composition and function were observed between liver graft preservation methods. Future research with larger randomized cohorts is needed to explore whether the NMP-associated shift in gut microbiota impacts clinical outcomes and if breath VOCs could serve as biomarkers of the clinical trajectory in liver transplant patients.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"284-294"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Characteristics, Treatment Effects and Risk Factors of Liver Cirrhosis in Patients with Wilson's Disease Hepatic Type.","authors":"Yu-Jia Lu, Chuan-Su Yuan, Yue-Yang Ma, Ke-Ying Ou, Du-Xian Liu, Bin Liu, Yong-Feng Yang, Qing-Fang Xiong","doi":"10.14218/JCTH.2024.00453","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00453","url":null,"abstract":"<p><strong>Background and aims: </strong>Wilson's disease (WD) is a rare autosomal recessive genetic disorder that can be treated with medications. The lack of a single, specific diagnostic indicator leads to diagnostic difficulties, which may result in disease progression to cirrhosis and even liver cancer. Thus, this study aimed to analyze the clinical data, imaging, histopathological manifestations, genetic testing results, and treatment effects of patients with WD hepatic type, and to explore the factors related to WD cirrhosis.</p><p><strong>Methods: </strong>A single-center retrospective study was performed. 48 WD patients with a Leipzig score ≥ 4 were divided into a cirrhosis group and a non-cirrhosis group based on the presence of cirrhosis. Logistic regression analysis and odds ratios were used to describe the strength of association between risk factors and cirrhosis. The predictive value of the model for cirrhosis occurrence was evaluated by calculating the area under the receiver operating characteristic curve and the cutoff value.</p><p><strong>Results: </strong>All 48 patients diagnosed with WD had liver damage, with males accounting for 54.17%. The median age at diagnosis was 28 years (range: 10.25-40.5 years), and 39.58% of patients had cirrhosis. The most prevalent mutation was c.2333G>T (p.Arg778Leu), found in 41.30% (19/46) of cases. Imaging revealed fatty liver in 31.25% (15/48) of patients and \"honeycomb-like\" cirrhosis nodules in 73.68% (14/19). Compared with the non-cirrhosis group, the cirrhosis group had a higher positive rate for the Kayser-Fleischer (K-F) ring, older age at diagnosis, and higher levels of immunoglobulin G, but lower levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, white blood cells, and platelets (<i>p</i> < 0.05). Age at diagnosis (odds ratio = 1.072, 95% confidence interval = 1.007-1.142, <i>p</i> = 0.03) and the K-F ring (odds ratio = 18.657, 95% confidence interval = 1.451-239.924, <i>p</i> = 0.025) were independent risk factors for WD-related cirrhosis. The best values of area under the receiver operating characteristic curve for age at diagnosis combined with the K-F ring in predicting WD cirrhosis were 0.909. The average follow-up time for 33 patients was 48.6 months (range: 12-72 months). The biochemical recovery rate was over 60% after 12-72 months of treatment with zinc gluconate and/or penicillamine.</p><p><strong>Conclusions: </strong>Age at diagnosis, combined with the K-F ring, is a simple and effective risk factor for WD-related cirrhosis. Zinc gluconate and penicillamine are safe and effective treatments.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"306-314"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ursolic Acid Modulates Estrogen Conversion to Relieve Inflammation in Metabolic Dysfunction-associated Steatotic Liver Disease via HSD17B14.","authors":"Simin Gu, Hui Zhang, Zhekun Xiong, Chong Chen, Junmin Wang, Dan Fang, Yiyuan Zheng, Yong Li","doi":"10.14218/JCTH.2024.00414","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00414","url":null,"abstract":"<p><strong>Background and aims: </strong>The incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) has been escalating annually, positioning it as the leading cause of chronic liver disease worldwide. Ursolic acid has demonstrated promising therapeutic efficacy in managing MASLD, thereby justifying the need for an in-depth exploration of its pharmacological mechanisms. This study aimed to investigate elucidate the therapeutic mechanisms by which ursolic acid modulates estrogen conversion in the treatment of MASLD.</p><p><strong>Methods: </strong>Building upon prior studies that have highlighted the potent anti-inflammatory effects of ursolic acid and its specific targeting of 17β-hydroxysteroid dehydrogenase 14 (HSD17B14), this investigation employed a western diet to induce MASLD in murine models with varying severities over different time intervals.</p><p><strong>Results: </strong>The protein expression of HSD17B14 initially increased, followed by a subsequent decrease. This trend was accompanied by corresponding changes in 17β-estradiol (E2) and estrone (E1) levels. Intervention with ursolic acid resulted in a reduction in HSD17B14 and E1 levels during the phase of high HSD17B14 expression, while simultaneously elevating E2 levels. In steatotic hepatocytes, E1 promoted cellular inflammation, whereas E2 exhibited anti-inflammatory effects. However, the alleviated effects of E2 were antagonized by HSD17B14. As expected, ursolic acid modulated HSD17B14, thereby mitigating the inflammatory response in steatotic hepatocytes.</p><p><strong>Conclusions: </strong>HSD17B14, a crucial enzyme regulating the balance between E1 and E2, catalyzes the conversion of estrogen E2 into E1, thereby exacerbating tissue inflammation induced by metabolic stress. Ursolic acid, by modulating HSD17B14-mediated estrogen conversion, appears to ameliorate immune-related inflammation in MASLD.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"269-277"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liver Injury in Immune Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Five New Classification Types.","authors":"Rolf Teschke","doi":"10.14218/JCTH.2024.00402","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00402","url":null,"abstract":"<p><p>Liver injury in Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) is a multifaceted disorder, lacking cohort homogeneity due to a variety of potential causes, including drugs, arsenic and other heavy metals, glyphosate, infections, and ultraviolet radiation. The goals of this review were (1) to analyze the role of diagnostic algorithms in assessing causality for potential culprits involved in the development of liver injury associated with immune-mediated SJS and TEN, which represent immune-based variant disorders within a continuous spectrum. Milder forms are classified as SJS or SJS/TEN overlap, while TEN is known as the most serious form; and (2) to interpret the findings that allow for the characterization of the different types of these disorders. The manuscript is based on an extensive literature search for single case reports, case cohorts, and review articles. Search terms included: Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, and specific diagnostic algorithms such as the Roussel Uclaf Causality Assessment Method (RUCAM) and the Algorithm of Drug Causality for Epidermal Necrolysis (ALDEN). For the purpose of basic feature description, the uniform term SJS/TEN is used in the current analysis. SJS/TEN presents with five different cohort types: SJS/TEN type (1), which refers to a cohort of SJS/TEN caused by drugs, as assessed by both ALDEN and RUCAM; type (2), representing SJS/TEN due to drugs and assessed by ALDEN only, but not by RUCAM; type (3), which includes a cohort of SJS/TEN caused by drugs, assessed by non-ALDEN and non-RUCAM tools; type (4), which focuses on a cohort of SJS/TEN caused by non-drug culprits, assessed by various tools; and type (5), which considers a cohort of SJS/TEN caused by unknown culprits. Using this new SJS/TEN typology will help better characterize individual features, personalize treatment, and clarify pathogenetic specifics for each of the five disease types. This new SJS/TEN typology provides clarity by replacing issues of inhomogeneity with cohort homogeneity.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"339-357"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocellular Carcinoma and the Role of Liver Transplantation: An Update and Review.","authors":"Lynette M Sequeira, N Begum Ozturk, Leandro Sierra, Merve Gurakar, Merih Deniz Toruner, Melanie Zheng, Cem Simsek, Ahmet Gurakar, Amy K Kim","doi":"10.14218/JCTH.2024.00432","DOIUrl":"https://doi.org/10.14218/JCTH.2024.00432","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death worldwide. Multiple treatment modalities are available for the management of HCC, depending on its stage as determined by the Barcelona Clinic Liver Cancer staging system. Because liver transplantation (LT) theoretically removes the cancer and replaces the organ at risk for future malignancy, LT is often considered the most definitive and one of the most efficacious treatment options for HCC. Nevertheless, the success and efficacy of liver transplantation depend on various tumor characteristics. As a result, multiple criteria have been developed to assess the appropriateness of a case of HCC for LT, with the pioneering Milan Criteria established in 1996. Over the past 20 to 30 years, these criteria have been critically evaluated, expanded, and often liberalized to make LT for patients with HCC a more universally applicable option. Furthermore, the development of other treatment modalities has enabled downstaging and bridging strategies for HCC prior to LT. In this narrative and comprehensive review, we provided an update on recent trends in the epidemiology of HCC, selection criteria for LT, implementation of LT across different regions, treatment modalities available as bridges, downstaging strategies, alternatives to LT, and, finally, post-LT surveillance.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 4","pages":"327-338"},"PeriodicalIF":3.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patients with AMA/anti-sp100/anti-gp210 Positivity and Cholestasis Can Manifest Conditions Beyond Primary Biliary Cholangitis.","authors":"Xin Zeng, Tingting Lv, Shuxiang Li, Sha Chen, Buer Li, Zhijiao Lu, Yu Wang, Xiaojuan Ou, Xinyan Zhao, Hong You, Weijia Duan, Jidong Jia","doi":"10.14218/JCTH.2024.00374","DOIUrl":"10.14218/JCTH.2024.00374","url":null,"abstract":"<p><strong>Background and aims: </strong>The diagnostic value of primary biliary cholangitis (PBC)-specific antibodies in patients with elevated alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) levels, and other identifiable causes, was unclear. Our study aimed to determine whether etiological treatments in PBC-specific antibody-positive patients could improve liver biochemical tests, thereby distinguishing them from individuals with PBC.</p><p><strong>Methods: </strong>We enrolled patients who were positive for PBC-specific antibodies and elevated ALP and/or GGT levels but with other identifiable etiologies. Changes in liver biochemistry following non-ursodeoxycholic acid etiological treatments were monitored.</p><p><strong>Results: </strong>A total of 155 patients with positive PBC-specific antibodies and elevated ALP and/or GGT levels due to non-PBC diseases were enrolled. Among them, 100 patients were diagnosed with non-PBC liver diseases, mainly metabolic-associated fatty liver disease, drug-induced liver injury, and autoimmune hepatitis. Additionally, 55 patients had non-liver diseases, predominantly connective tissue diseases. The median follow-up duration was 15.9 (4.7-25.6) months. Among 141 patients who completed follow-up after receiving etiological treatments, 85.1% (120/141) showed improvement in ALP and/or GGT levels, with 51.8% (73/141) achieving normalization of both ALP and GGT. However, 68 patients continued to exhibit elevated ALP and/or GGT, with 55 patients displaying isolated GGT elevation and 11 patients showing liver histological changes not consistent with PBC.</p><p><strong>Conclusions: </strong>PBC-specific antibodies, along with elevated ALP and GGT levels, may occur in various non-PBC diseases. Etiological treatments may improve or even resolve cholestatic biochemistry. For these patients, initiating etiological treatment rather than immediately starting ursodeoxycholic acid therapy would be justified.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"200-206"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chinese Guidelines on the Management of Hepatic Encephalopathy in Cirrhosis (2024).","authors":"Xiaoyuan Xu, Huiguo Ding, Wengang Li, Ying Han, Yujuan Guan, Jinghang Xu, Yifan Han, Jidong Jia, Lai Wei, Zhongping Duan, Yuemin Nan, Hui Zhuang","doi":"10.14218/JCTH.2024.00484","DOIUrl":"10.14218/JCTH.2024.00484","url":null,"abstract":"<p><p>With progress in basic and clinical research on hepatic encephalopathy in cirrhosis worldwide, the Chinese Society of Hepatology of the Chinese Medical Association has invited experts in relevant fields to revise the 2018 \"Chinese Guidelines on the Management of Hepatic Encephalopathy in Cirrhosis.\" The updated guidelines provide recommendations for the clinical diagnosis, treatment, and both primary and secondary prevention of hepatic encephalopathy in cirrhosis.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"253-267"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SOX9 Overexpression Ameliorates Metabolic Dysfunction-associated Steatohepatitis Through Activation of the AMPK Pathway.","authors":"Juan Deng, Kai Ding, Shuqing Liu, Fei Chen, Ru Huang, Bonan Xu, Xin Zhang, Weifen Xie","doi":"10.14218/JCTH.2024.00197","DOIUrl":"10.14218/JCTH.2024.00197","url":null,"abstract":"<p><strong>Background and aims: </strong>The transcription factor sex-determining region Y-related high-mobility group-box gene 9 (SOX9) plays a critical role in organ development. Although SOX9 has been implicated in regulating lipid metabolism <i>in vitro</i>, its specific role in metabolic dysfunction-associated steatohepatitis (MASH) remains poorly understood. This study aimed to investigate the role of SOX9 in MASH pathogenesis and explored the underlying mechanisms.</p><p><strong>Methods: </strong>MASH models were established using mice fed either a methionine- and choline-deficient (MCD) diet or a high-fat, high-fructose diet. To evaluate the effects of SOX9, hepatocyte-specific SOX9 deletion or overexpression was performed. Lipidomic analyses were conducted to assess how SOX9 influences hepatic lipid metabolism. RNA sequencing was employed to identify pathways modulated by SOX9 during MASH progression. To elucidate the mechanism further, HepG2 cells were treated with an adenosine monophosphate-activated protein kinase (AMPK) inhibitor to test whether SOX9 acts via AMPK activation.</p><p><strong>Results: </strong>SOX9 expression was significantly elevated in hepatocytes of MASH mice. Hepatocyte-specific SOX9 deletion exacerbated MCD-induced MASH, whereas overexpression of SOX9 mitigated high-fat, high-fructose-induced MASH. Lipidomic and RNA sequencing analyses revealed that SOX9 suppresses the expression of genes associated with lipid metabolism, inflammation, and fibrosis in MCD-fed mice. Furthermore, SOX9 deletion inhibited AMPK pathway activation, while SOX9 overexpression enhanced it. Notably, administration of an AMPK inhibitor negated the protective effects of SOX9 overexpression, leading to increased lipid accumulation in HepG2 cells.</p><p><strong>Conclusions: </strong>Our findings demonstrate that SOX9 overexpression alleviates hepatic lipid accumulation in MASH by activating the AMPK pathway. These results highlight SOX9 as a promising therapeutic target for treating MASH.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"189-199"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Solute Carrier Family Transporters in Hepatic Steatosis and Hepatic Fibrosis.","authors":"Chi Zhang, Xuanran Yang, Yi Xue, Huan Li, Chuanfei Zeng, Mingkai Chen","doi":"10.14218/JCTH.2024.00348","DOIUrl":"10.14218/JCTH.2024.00348","url":null,"abstract":"<p><p>Solute carrier (SLC) family transporters are crucial transmembrane proteins responsible for transporting various molecules, including amino acids, electrolytes, fatty acids, and nucleotides. To date, more than fifty SLC transporter subfamilies have been identified, many of which are linked to the progression of hepatic steatosis and fibrosis. These conditions are often caused by factors such as non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, which are major contributors to the global liver disease burden. The activity of SLC members regulates the transport of substrates across biological membranes, playing key roles in lipid synthesis and metabolism, mitochondrial function, and ferroptosis. These processes, in turn, influence the function of hepatocytes, hepatic stellate cells, and macrophages, thereby contributing to the development of hepatic steatosis and fibrosis. Additionally, some SLC transporters are involved in drug transport, acting as critical regulators of drug-induced hepatic steatosis. Beyond substrate transport, certain SLC members also exhibit additional functions. Given the pivotal role of the SLC family in hepatic steatosis and fibrosis, this review aimed to summarize the molecular mechanisms through which SLC transporters influence these conditions.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"13 3","pages":"233-252"},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}