World Journal of Hepatology最新文献

{"title":"Yinchenhao decoction alleviates obstructive jaundice liver injury by modulating epidermal growth factor receptor and constitutive androstane receptor signaling.","authors":"Jun-Jian Liu, Han-Wei Mei, Yan-Yan Jing, Zhong-Lian Li, Su-Guo Wu, Hong-Xia Yuan, Xi-Bo Zhang","doi":"10.4254/wjh.v17.i3.101724","DOIUrl":"10.4254/wjh.v17.i3.101724","url":null,"abstract":"<p><strong>Background: </strong>Yinchenhao decoction (YCHD) is a traditional Chinese medicine widely used to treat liver damage caused by obstructive jaundice (OJ). Although YCHD has demonstrated protective effects against liver damage, reduced apoptosis, and mitigated oxidative stress in OJ, the precise molecular mechanisms involved remain poorly understood.</p><p><strong>Aim: </strong>To investigate the beneficial effects of YCHD on OJ and elucidate the underlying mechanisms.</p><p><strong>Methods: </strong>The active constituents of YCHD were identified using liquid chromatography-tandem mass spectrometry, and their potential targets for OJ treatment were predicted through network pharmacology. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed. An OJ rat model was established by common bile duct ligation. Rats were divided into three groups: Sham surgery (S Group), model (O Group), and YCHD (Y Group). YCHD was administered to Group Y for one week. Bilirubin levels, liver function parameters, and bile acid concentrations in blood and urine were measured by enzyme-linked immunosorbent assay. The bile acid renal clearance rate (Clr) was calculated. Histopathological evaluation of liver and kidney tissues was performed using hematoxylin-eosin staining. Western blotting was utilized to assess the expression of key bile acid metabolism and transport proteins in both liver and kidney tissues. The expression of the constitutive androstane receptor (CAR) and its nuclear localization were evaluated by immunohistochemistry. Molecular docking studies identified the epidermal growth factor receptor (EGFR) as a potential target of YCHD's active components. An OJ cell model was created using human liver (L02) and renal tubular epithelial (HK-2) cells, which were treated with YCHD-containing serum. Western blotting and immunofluorescence assays were employed to evaluate CAR expression and its nuclear localization in relation to EGFR activation.</p><p><strong>Results: </strong>Network analysis identified the EGFR signaling pathway as a key mechanism through which YCHD exerts its effects on OJ. <i>In vivo</i> experiments showed that YCHD improved liver function, reduced OJ-induced pathology in liver and kidney tissues, and decreased serum bile acid content by enhancing bile acid Clr and urine output. YCHD also increased CAR expression and nuclear heterotopy, upregulating proteins involved in bile acid metabolism and transport, including CYP3A4, UGT1A1, MRP3, and MRP4 in the liver, and MRP2 and MRP4 in the kidneys. In vitro, YCHD increased CAR expression and nuclear heterotopy in L02 and HK-2 cells, an effect that was reversed by EGFR agonists.</p><p><strong>Conclusion: </strong>YCHD enhances bile acid metabolism in the liver and promotes bile acid excretion in the kidneys, ameliorating liver damage caused by OJ. These effects are likely mediated by the upregulation of CAR and its nuclear translocation.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"101724"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of cardiovascular health metrics and metabolic associated fatty liver disease: Methodological limitations, and future directions.","authors":"Arunkumar Krishnan, Diptasree Mukherjee","doi":"10.4254/wjh.v17.i3.105635","DOIUrl":"10.4254/wjh.v17.i3.105635","url":null,"abstract":"<p><p>Metabolic-associated fatty liver disease (MAFLD), formerly known as nonalcoholic fatty liver disease, is an increasing global health challenge with substantial implications for metabolic and cardiovascular health (CVH). A recent study by Fu <i>et al</i> investigated the relationship between CVH metrics, specifically Life's Simple 7 and Life's Essential 8, and the prevalence of MAFLD. While this study offered important insights into the relationship between CVH and MAFLD, several methodological limitations, unaddressed confounding factors, and potential biases that could impact the interpretation of their findings should be considered. The study's cross-sectional nature restricted the ability to draw causal conclusions, and it did not fully account for potential confounding factors such as dietary habits, genetic predispositions, and medication use. Furthermore, relying on transient elastography to diagnose MAFLD introduces certain diagnostic limitations. Longitudinal study designs, advanced statistical modeling techniques, and diverse population groups should be utilized to strengthen future research. Exploring the mechanistic pathways that link CVH metrics to MAFLD through multi-omics approaches and interventional studies will be essential in formulating targeted prevention and treatment strategies. Structural equation modeling and machine learning techniques could provide a more refined analysis of these interrelated factors. Additionally, future research should employ longitudinal study designs and explore genetic and epigenetic influences to enhance our understanding of CVH and MAFLD interactions.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"105635"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota differences, metabolite changes, and disease intervention during metabolic - dysfunction - related fatty liver progression.","authors":"Jian-Zhong Shu, Yu-Han Huang, Xiao-Hong He, Feng-Ying Liu, Qian-Qian Liang, Xue-Tong Yong, Yong-Fang Xie","doi":"10.4254/wjh.v17.i3.103854","DOIUrl":"10.4254/wjh.v17.i3.103854","url":null,"abstract":"<p><p>In the current era, metabolic dysfunction-associated steatotic liver disease (MASLD) has gradually developed into a major type of chronic liver disease that is widespread globally. Numerous studies have shown that the gut microbiota plays a crucial and indispensable role in the progression of MASLD. Currently, the gut microbiota has become one of the important entry points for the research of this disease. Therefore, the aim of this review is to elaborate on the further associations between the gut microbiota and MASLD, including the changes and differences in the microbiota between the healthy liver and the diseased liver. Meanwhile, considering that metabolic dysfunction-associated fatty liver and metabolic dysfunction-associated steatohepatitis are abnormal pathological states in the development of the disease and that the liver exhibits different degrees of fibrosis (such as mild fibrosis and severe fibrosis) during the disease progression, we also conduct a comparison of the microbiota in these states and use them as markers of disease progression. It reveals the changes in the production and action mechanisms of short-chain fatty acids and bile acids brought about by changes in the gut microbiota, and the impact of lipopolysaccharide from Gram-negative bacteria on the disease. In addition, the regulation of the gut microbiota in disease and the production and inhibition of related disease factors by the use of probiotics (including new-generation probiotics) will be explored, which will help to monitor the disease progression of patients with different gut microbiota compositions in the future and carry out personalized targeted therapies for the gut microbiota. This will achieve important progress in preventing and combating this disease.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"103854"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic dysfunction-associated steatotic liver disease and omega-6 polyunsaturated fatty acids: Friends or foes.","authors":"Mona A Hegazy, Safaa M Ahmed, Shaimaa M Sultan, Osama F Afifi, Manal A Mohamed, Alshimaa E Azab, Mohamed A Hassanen, Rakan K Zaben","doi":"10.4254/wjh.v17.i3.102286","DOIUrl":"10.4254/wjh.v17.i3.102286","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide. Its prevalence is closely linked to the dramatic rise in obesity and non-communicable diseases. MASLD exhibits a progressive trajectory that may culminate in development of hepatic cirrhosis, thereby predisposing affected individuals to an elevated likelihood of hepatocarcinogenesis. Diet, especially dietary fatty acids, serves as a key link between nutrient intake and MASLD pathogenesis.</p><p><strong>Aim: </strong>To explore the impact of various omega-6 fatty acid subtypes on the pathogenesis and therapeutic strategies of MASLD.</p><p><strong>Methods: </strong>A systematic literature search was conducted across Web of Science, PubMed, Cochrane Central, Scopus, and Embase databases from inception through June 2024 to identify all original studies linking different subtypes of omega-6 polyunsaturated fatty acids to the pathogenesis and management of MASLD. The search strategy explored the linkage between omega-6 polyunsaturated fatty acids and their subtypes, including linoleic acid (LA), gamma-linolenic acid (GLA), arachidonic acid, conjugated LA, and docosapentaenoic acid, in relation to MASLD and cardiometabolic risk.</p><p><strong>Results: </strong>By employing the specified search strategy, a total of 83 articles were identified as potentially eligible. During the title, abstract, and full-text screening phases, 27 duplicate records were removed, leaving 56 records for relevance screening. Of these, 43 records were excluded for reasons such as irrelevance and language restrictions (limited to English), resulting in 13 full-text articles being included for detailed assessment (10 human studies,1 animal study, and 2 review articles). Although certain subtypes, as GLA, dihomo-GLA, omega-6-derived oxylipins, and most arachidonic acid-derived eicosanoids, exhibit pro-inflammatory effects, our findings suggest that other subtypes such as LA, cis-9, trans-11 conjugated LA, and docosapentaenoic acid have beneficial effects on fatty liver, cardiometabolic risk factors, and inflammation, even at high intake levels.</p><p><strong>Conclusion: </strong>The varying health effects of omega-6 fatty acids, ranging from anti-inflammatory to pro-inflammatory impacts on the liver, leave the question of their recommendation for MASLD patients unresolved. This underscores the importance of careful selection when considering omega-6 supplementation.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"102286"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of autoimmune phenomena in nonalcoholic fatty liver disease: Insights and limitations.","authors":"Arunkumar Krishnan, Diptasree Mukherjee","doi":"10.4254/wjh.v17.i3.103835","DOIUrl":"10.4254/wjh.v17.i3.103835","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease, previously known as nonalcoholic fatty liver disease (NAFLD), is becoming increasingly common and is associated with significant morbidity and mortality related to both liver and non-liver issues. In its early stages, NAFLD is characterized by immune cell dysregulation, which suggests that immune-targeted therapies could be a viable treatment option for nonalcoholic steatohepatitis. A recent study by Zhu <i>et al</i>. investigated the role of autoantibodies in metabolic dysfunction-associated steatotic liver disease at various histological stages. While the research provided valuable insights, several methodological concerns are noted, which include the study's retrospective design, a limited panel of autoantibodies, and a lack of a prospective study design that adequately controls for confounding factors such as age, comorbidities and lifestyle. Furthermore, the interpretation of positive antinuclear antibodies as evidence of autoimmune involvement in NAFLD is questioned due to the possibility of nonspecific immune responses. Recommendations to improve the study's design include conducting prospective studies, implementing more detailed antibody profiling, and adjusting for demographic and clinical factors. Future studies should address these issues to improve the clinical relevance and credibility of findings related to autoimmunity in NAFLD.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"103835"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota in the development and progression of chronic liver diseases: Gut microbiota-liver axis.","authors":"Aysun Yakut","doi":"10.4254/wjh.v17.i3.104167","DOIUrl":"10.4254/wjh.v17.i3.104167","url":null,"abstract":"<p><p>The gut microbiota (GM) is a highly dynamic ecology whose density and composition can be influenced by a wide range of internal and external factors. Thus, \"How do GM, which can have commensal, pathological, and mutualistic relationships with us, affect human health?\" has become the most popular research issue in recent years. Numerous studies have demonstrated that the trillions of microorganisms that inhabit the human body can alter host physiology in a variety of systems, such as metabolism, immunology, cardiovascular health, and neurons. The GM may have a role in the development of a number of clinical disorders by producing bioactive peptides, including neurotransmitters, short-chain fatty acids, branched-chain amino acids, intestinal hormones, and secondary bile acid conversion. These bioactive peptides enter the portal circulatory system through the gut-liver axis and play a role in the development of chronic liver diseases, cirrhosis, and hepatic encephalopathy. This procedure is still unclear and quite complex. In this study, we aim to discuss the contribution of GM to the development of liver diseases, its effects on the progression of existing chronic liver disease, and to address the basic mechanisms of the intestinal microbiota-liver axis in the light of recent publications that may inspire the future.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"104167"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mogroside V protects against acetaminophen-induced liver injury by reducing reactive oxygen species and c-jun-N-terminal kinase activation in mice.","authors":"Jia-Lin Shi, Tian Sun, Qing Li, Chun-Mei Li, Jun-Fei Jin, Chong Zhang","doi":"10.4254/wjh.v17.i3.104520","DOIUrl":"10.4254/wjh.v17.i3.104520","url":null,"abstract":"<p><strong>Background: </strong>High levels of acetaminophen (APAP) consumption can result in significant liver toxicity. Mogroside V (MV) is a bioactive, plant-derived triterpenoid known for its various pharmacological activities. However, the impact of MV on acute liver injury (ALI) is unknown.</p><p><strong>Aim: </strong>To investigate the hepatoprotective potential of MV against liver damage caused by APAP and to examine the underlying mechanisms.</p><p><strong>Methods: </strong>Mice were divided into three groups: Saline, APAP and APAP + MV. MV (10 mg/kg) was given intraperitoneally one hour before APAP (300 mg/kg) administration. Twenty-four hours after APAP exposure, serum transaminase levels, liver necrotic area, inflammatory responses, nitrotyrosine accumulation, and c-jun-N-terminal kinase (JNK) activation were assessed. Additionally, we analyzed reactive oxygen species (ROS) levels, JNK activation, and cell death in alpha mouse liver 12 (AML12) cells.</p><p><strong>Results: </strong>MV pre-treatment <i>in vivo</i> led to a reduction in the rise of aspartate transaminase and alanine transaminase levels, mitigated liver damage, decreased nitrotyrosine accumulation, and blocked JNK phosphorylation resulting from APAP exposure, without affecting glutathione production. Similarly, MV diminished the APAP-induced increase in ROS, JNK phosphorylation, and cell death <i>in vitro</i>.</p><p><strong>Conclusion: </strong>Our study suggests that MV treatment alleviates APAP-induced ALI by reducing ROS and JNK activation.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"104520"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypochloremia is an underutilised prognostic marker in patients with advanced liver cirrhosis and liver failure.","authors":"Jinit R Soni, Sudheer Marrapu, Ramesh Kumar","doi":"10.4254/wjh.v17.i3.103807","DOIUrl":"10.4254/wjh.v17.i3.103807","url":null,"abstract":"<p><p>Patients with advanced liver cirrhosis and liver failure frequently experience abnormalities in their serum electrolyte levels. In such patients, hyponatremia has been identified as a predictor of poor outcomes. However, emerging evidence suggests that serum chloride may provide even better prognostic information in similar situations. Hypochloremia, characterised by low serum chloride levels, has been linked to increased mortality, exacerbated organ dysfunction, and higher requirements for renal replacement therapy and vasopressors in various critical conditions, including advanced liver diseases. The pathophysiological mechanisms underlying the association between low serum chloride levels and poor outcomes in liver disease appear to involve complex interactions among electrolyte imbalances, renal function, and systemic hemodynamics. Chloride dysregulation can influence renal salt-sensing mechanisms, disrupt acid-base homeostasis, and exacerbate complications such as hepatic encephalopathy and hepatorenal syndrome. This article aims to elucidate the prognostic significance of lower serum chloride levels in patients with advanced liver disease. By reviewing recent literature and analysing clinical data, we seek to establish serum chloride as an underutilised but valuable prognostic marker. Understanding the role of serum chloride in liver disease could enhance prognostic accuracy, refine treatment strategies, and ultimately improve patient outcomes.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"103807"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress on the roles of complement in liver injury.","authors":"Li-Li Ou, Jin-Lian Jiang, Man-Lu Guo, Jin-Hua Wu, Wei-Wei Zhong, Yi-Huai He","doi":"10.4254/wjh.v17.i3.103839","DOIUrl":"10.4254/wjh.v17.i3.103839","url":null,"abstract":"<p><p>The complement system is crucial for maintaining immunological homeostasis in the liver, playing a significant role in both innate and adaptive immune responses. Dysregulation of this system is closely linked to the pathogenesis of various liver diseases. Modulating the complement system can affect the progression of these conditions. To provide insights into treating liver injury by targeting the regulation of the complement system, we conducted a comprehensive search of major biomedical databases, including MEDLINE, PubMed, EMBASE, and Web of Science, to identify articles on complement and liver injury and reviewed the functions and mechanisms of the complement system in liver injury.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"103839"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune cells in metabolic associated fatty liver disease: Global trends and hotspots (2004-2024).","authors":"Wen-Ying Qi, Shi-Hao Zheng, Si-Ze Li, Wei Wang, Qiu-Yue Wang, Qi-Yao Liu, Xiao-Ke Li, Jia-Xin Zhang, Da-Nan Gan, Yong-An Ye, Xiao-Bin Zao","doi":"10.4254/wjh.v17.i3.103327","DOIUrl":"10.4254/wjh.v17.i3.103327","url":null,"abstract":"<p><strong>Background: </strong>The interplay between immune cells and metabolic associated fatty liver disease (MAFLD) is a critical research frontier, bridging immunology and hepatology. The bibliometric findings can guide future research and funding priorities in the field by highlighting key areas of focus and potential therapeutic targets.</p><p><strong>Aim: </strong>To analyze the literature on immune cells and MAFLD, identifying research trends and future hotspots.</p><p><strong>Methods: </strong>A systematic search in the Web of Science Core Collection from January 1, 2004 to May 20, 2024, yielded 1936 articles on immune cells and MAFLD. Excluding non-research documents, the data were analyzed using R packages Cluster profiler, enrichplot, ggplot2, VOSviewer and CiteSpace. Visualizations were created for countries, institutions, authors, journals, fields, co-cited references, keywords, genes, and diseases, with gene a disease data from Citexs.</p><p><strong>Results: </strong>The field gained momentum in 2006, with the United States of America and China as leading contributors. Key research themes included oxidative stress, metabolic syndrome, liver fibrosis, and the role of Kupffer cells. Bioinformatics identified interleukin-6, tumor necrosis factor and signal transducer and activator of transcription 3 as central proteins in immune responses and inflammation, suggesting potential therapeutic targets for MAFLD. Clinically, these hub genes play pivotal roles in the pathogenesis of MAFLD. For instance, targeting the tumor necrosis factor signaling pathway could reduce inflammation, while modulating interleukin-6 and signal transducer and activator of transcription 3 expression may improve metabolic function, offering new strategies for MAFLD therapy.</p><p><strong>Conclusion: </strong>This bibliometric analysis reports on the research hotspots and emerging trends in the field of immune cells and MAFLD, highlighting key proteins and potential therapeutic strategies through bioinformatics.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 3","pages":"103327"},"PeriodicalIF":2.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}