Annals of hepatology最新文献_第6页

Lipocalin-2 silencing alleviates sepsis-induced liver injury through inhibition of ferroptosis Lipocalin-2沉默通过抑制铁下垂减轻败血症诱导的肝损伤。

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2024.101756

Yuping Li , Lu Li , Yuming Zhang , Qi Yun , Ruoli Du , Hongwei Ye , Zhenghong Li , Qin Gao

{"title":"Lipocalin-2 silencing alleviates sepsis-induced liver injury through inhibition of ferroptosis","authors":"Yuping Li , Lu Li , Yuming Zhang , Qi Yun , Ruoli Du , Hongwei Ye , Zhenghong Li , Qin Gao","doi":"10.1016/j.aohep.2024.101756","DOIUrl":"10.1016/j.aohep.2024.101756","url":null,"abstract":"<div><h3>Introduction and Objectives</h3><div>Liver plays a key role in sepsis, a systemic inflammatory response syndrome caused by infection. Ferroptosis is involved in sepsis-induced liver injury. We aimed to assess the changes in ferroptosis in cecal ligation and puncture (CLP)-induced septic mice, and determine the role of lipocalin-2 (LCN2) in liver ferroptosis.</div></div><div><h3>Materials and Methods</h3><div>CLP was used to induce sepsis in mice. The morphological changes in liver tissues and mitochondrial structure were observed using hematoxylin and eosin staining and transmission electron microscopy. The levels of serum alanine transaminase, aspartate aminotransferase, superoxide dismutase, and malondialdehyde were detected using the corresponding kits. The changes of reactive oxygen species level in liver tissues were detected using dihydroethidium as a fluorescence probe. LCN2, cysteine-glutamate reverse transport system, and dihydroorotate dehydrogenase protein levels in the liver were detected by western blotting. The ferroptosis inhibitor ferrostatin-1 (Fer-1), iron chelator dexrazoxane (DXZ), iron-dextran, and LCN2 knockdown studies were performed to determine role of ferroptosis and LCN2 in liver injury during sepsis.</div></div><div><h3>Results</h3><div>Ferroptosis levels increased in the liver tissues of CLP-induced septic mice. Both Fer-1 and DXZ suppressed ferroptosis and attenuated liver injury following sepsis challenge, whereas iron-dextran increased ferroptosis and liver injury in mice with sepsis. LCN2 knockdown suppressed ferroptosis and reduced oxidative stress in the liver.</div></div><div><h3>Conclusions</h3><div>Ferroptosis inhibition attenuates septic liver injury. LCN2 knockdown alleviates sepsis-induced liver injury by inhibiting ferroptosis and reducing oxidative stress.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101756"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811698","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}

引用次数: 0

One-stop shop endoscopy for patients with biliary pancreatitis: A Jack of all trades? 胆道性胰腺炎患者的一站式内窥镜检查：多面手？

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2024.101752

Łukasz Krupa , Frank Lammert , Marcin Krawczyk

引用次数: 0

Racial and ethnic disparities in alcohol-associated liver disease hospitalizations in Brazil before and after the COVID-19 pandemic COVID-19大流行前后巴西酒精相关肝病住院的种族和民族差异

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2024.101742

Daniel L Heringer , Gabriel P.A. Costa , Jeremy Weleff , Victor Rodrigues , Shreya Sengupta , Akhil Anand

{"title":"Racial and ethnic disparities in alcohol-associated liver disease hospitalizations in Brazil before and after the COVID-19 pandemic","authors":"Daniel L Heringer , Gabriel P.A. Costa , Jeremy Weleff , Victor Rodrigues , Shreya Sengupta , Akhil Anand","doi":"10.1016/j.aohep.2024.101742","DOIUrl":"10.1016/j.aohep.2024.101742","url":null,"abstract":"<div><h3>Introduction and Objectives</h3><div>The COVID-19 pandemic has resulted in a greater incidence of alcohol-associated liver disease (ALD) and simultaneously magnified health-related inequalities. We evaluated the impact of race and ethnicity on ALD-related hospitalizations in Brazil.</div></div><div><h3>Materials and Methods</h3><div>An interrupted time series analysis was used to estimate ALD-related hospitalization in public hospitals in Brazil. Monthly hospitalization rates for 34 consecutive months before and after the point of interruption (March 2020) were calculated using the Sistema de Informações Hospitalares database across four ethnic groups: Black, Pardo, Black, and Pardo combined, and Others (White and Unknown Ethnicity).</div></div><div><h3>Results</h3><div>A total of 84,787 ALD-related hospitalizations were recorded during the study period. The mean age of hospitalized patients was 53 years (SD=12.5); 83.6% were male. Immediately after the start of the pandemic, there was a statistically significant decrease in monthly ALD-related hospitalization rates for the whole population and for all ethnic groups. Subsequently, compared to pre-pandemic rates, there was a statistically significant trend increase in the referred hospitalization rates for the total population (0.065, 95% CI= 0.045 to 0.085, p<0.01), black population (0.0028, 95% CI= 0.006 to 0.050, p<0.05), pardo population (0.077, 95% CI= 0.063 to 0.090, p<0.01), and for black and pardo combined population (0.066, 95% CI= 0.053 to 0.079, p<0.01); however, the increase in hospitalization rates among the Others population (0.059, 95% CI= -0,014 to 0.133, p>0.1) was not statistically significant.</div></div><div><h3>Conclusions</h3><div>The pandemic impacted ALD-related monthly hospitalization rates and disproportionately impacted Black and Pardo populations in Brazil.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101742"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142798670","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}

引用次数: 0

Mechanisms and therapeutic targets of mitochondria in the progression of metabolic dysfunction-associated steatotic liver disease 线粒体在代谢功能障碍相关脂肪变性肝病进展中的机制和治疗靶点

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2024.101774

Chenyang Mu , Sijie Wang , Zenghan Wang , Jian Tan , Haozan Yin , Yuefan Wang , Zhihui Dai , Dongyang Ding , Fu Yang

{"title":"Mechanisms and therapeutic targets of mitochondria in the progression of metabolic dysfunction-associated steatotic liver disease","authors":"Chenyang Mu , Sijie Wang , Zenghan Wang , Jian Tan , Haozan Yin , Yuefan Wang , Zhihui Dai , Dongyang Ding , Fu Yang","doi":"10.1016/j.aohep.2024.101774","DOIUrl":"10.1016/j.aohep.2024.101774","url":null,"abstract":"<div><div>Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) includes liver disease processes from simple fatty liver to nonalcoholic steatohepatitis, which may progress to liver fibrosis, cirrhosis, and even hepatocellular carcinoma (HCC). As the incidence of HCC derived from viral hepatitis decreases, MASLD has emerged as a significant health threat, driven by lifestyle changes and rising obesity rates among patients. The pathogenesis of MASLD is complex, involving factors such as insulin resistance, gut microbiota imbalance, and genetic and epigenetic factors. In recent years, the role of mitochondrial dysfunction in MASLD has gained significant attention, involving β-oxidation imbalance, oxidative stress increase, mitophagy defects, and mitochondrial DNA (mtDNA) mutations. This article reviews the pathophysiological mechanisms of mitochondrial dysfunction in MASLD, diagnostic methods, and potential therapeutic strategies. By synthesizing current research findings, the review aims to highlight the critical role of mitochondrial dysfunction as a target for future diagnostic and therapeutic interventions. This focus could pave the way for innovative clinical strategies, ultimately improving treatment options and patient prognosis in MASLD.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101774"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863158","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}

引用次数: 0

Outcomes and risk factors for de novo major depressive disorder after liver transplantation: Nested case-control study

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2025.101779

Young Jin Yoo , Jinhee Lee , Deok-Gie Kim , Minyu Kang , Hwa-hee Koh , Eun-Ki Min , Jae Geun Lee , Myoung Soo Kim , Dong Jin Joo

{"title":"Outcomes and risk factors for de novo major depressive disorder after liver transplantation: Nested case-control study","authors":"Young Jin Yoo , Jinhee Lee , Deok-Gie Kim , Minyu Kang , Hwa-hee Koh , Eun-Ki Min , Jae Geun Lee , Myoung Soo Kim , Dong Jin Joo","doi":"10.1016/j.aohep.2025.101779","DOIUrl":"10.1016/j.aohep.2025.101779","url":null,"abstract":"<div><h3>Introduction and Objectives</h3><div>Major depressive disorder (MDD) is a major psychiatric complication of liver transplantation (LT). Here, we aimed to analyze the impact of <em>de novo</em> MDD on survival post-LT and identify risk factors for this disorder among LT recipients.</div></div><div><h3>Materials and Methods</h3><div>A retrospective analysis was conducted on 1350 LT recipients at Severance Hospital, Korea, from July 2005 to December 2022. Patients with MDD were matched 1:5 with controls using a nested case-control design to control for immortal time bias.</div></div><div><h3>Results</h3><div>During follow-up post-LT, 58 patients (4.3 %) were newly diagnosed with MDD. The median time from LT to MDD diagnosis was 316 (interquartile range 46–920) days. Patients with MDD had significantly lower graft survival rates than controls at 1, 3, and 5 years after matching (89.5 %, 75.3 %, and 66.5 % vs. 95.5 %, 91.5 %, and 86.4 %, respectively; <em>P</em> = 0.003). Multivariable Cox regression identified <em>de novo</em> MDD as an independent risk factor for reduced graft survival (hazard ratio 2.39, 95 % confidence interval [CI] 1.15–4.98, <em>P</em> = 0.003). Independent risk factors for <em>de novo</em> MDD included female sex (odds ratio [OR] 2.29, 95 % CI 1.16–4.53, <em>P</em> = 0.017), alcoholic liver disease (OR 2.36, 95 % CI 1.16–4.75, <em>P</em> = 0.016), pre-transplant encephalopathy (OR 2.95, 95 % CI 1.49–5.79, <em>P</em> = 0.002), and lower hemoglobin levels (OR 0.85, 95 % CI 0.73–0.98, <em>P</em> = 0.025).</div></div><div><h3>Conclusions</h3><div>In our matched population of nested case controls, <em>de novo</em> MDD significantly reduced the survival of LT recipients. Screening and early intervention are required for LT recipients with risk factors for MDD.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101779"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603651","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}

引用次数: 0

Energy metabolism: An emerging therapeutic frontier in liver fibrosis

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2025.101896

Iram Irshad , Saleh A Alqahtani , Kenichi Ikejima , Ming-Lung Yu , Manuel Romero-Gomez , Mohammed Eslam

{"title":"Energy metabolism: An emerging therapeutic frontier in liver fibrosis","authors":"Iram Irshad , Saleh A Alqahtani , Kenichi Ikejima , Ming-Lung Yu , Manuel Romero-Gomez , Mohammed Eslam","doi":"10.1016/j.aohep.2025.101896","DOIUrl":"10.1016/j.aohep.2025.101896","url":null,"abstract":"<div><div>Liver fibrosis is a progressive response to chronic liver diseases characterized by a wound-healing process that leads to the accumulation of fibrillary extracellular matrix (ECM) proteins in and around the liver tissue. If left untreated, liver fibrosis can advance to cirrhosis and ultimately result in liver failure. Although there have been significant advancements in understanding the molecular mechanisms involved in liver fibrosis, effective therapeutic strategies to reverse or halt the condition remain limited. Recent research has underscored the critical role of energy metabolism in the initiation and progression of liver fibrosis. In response to liver injury, hepatic cells undergo metabolic reprogramming to meet the energy demands of myofibroblasts. This reprogramming involves various metabolic changes, including mitochondrial dysfunction, alterations in cellular bioenergetics, shifts in glycolysis and oxidative phosphorylation, as well as changes in lipid metabolism. These modifications can disrupt cellular energy homeostasis and increase energy release, activating hepatic cells, primarily hepatic stellate cells (HSCs). Activated HSCs then stimulate fibrogenic pathways, leading to the accumulation of ECM proteins in the liver, which exacerbates the progression of fibrosis.</div><div>This review aims to explore the emerging connection between energy metabolism and liver fibrosis, focusing on the metabolic alterations and molecular mechanisms that drive this condition. We also examine the therapeutic implications of modulating energy metabolism to reduce energy release and mitigate liver fibrosis. Altering energy metabolism to decrease energy release may represent a promising approach for treating liver fibrosis and chronic liver diseases.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101896"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584393","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}

引用次数: 0

Free fatty acid-induced DDX3 inhibits autophagy via miR-141 upregulation in diet-induced MASLD mice model system 在饮食诱导的MASLD小鼠模型系统中，游离脂肪酸诱导的DDX3通过上调miR-141抑制自噬。

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2024.101758

Md. Musa Hossain , Amit K. Mishra , Ajay K. Yadav , Md. Ismail , Teja Naveen Sata , Amrendra K. Sah , Arnab Banik , Gopal Sharma , Senthil K. Venugopal

{"title":"Free fatty acid-induced DDX3 inhibits autophagy via miR-141 upregulation in diet-induced MASLD mice model system","authors":"Md. Musa Hossain , Amit K. Mishra , Ajay K. Yadav , Md. Ismail , Teja Naveen Sata , Amrendra K. Sah , Arnab Banik , Gopal Sharma , Senthil K. Venugopal","doi":"10.1016/j.aohep.2024.101758","DOIUrl":"10.1016/j.aohep.2024.101758","url":null,"abstract":"<div><h3>Introduction and Objectives</h3><div>Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the primary causes of chronic liver disease and may lead to liver cirrhosis and hepatocellular carcinoma. Recent reports suggested that DEAD-box RNA helicase (DDX3) acts as a sensor of free fat accumulation and may modulate the pathogenesis via miRNAs. Hence, we hypothesized that DDX3 might modulate MASLD progression via miRNA-141-mediated inhibition of Sirt-1 and autophagy.</div></div><div><h3>Materials and Methods</h3><div>RNA and total protein were isolated from free fatty acid-treated HepG2 cells or CDAA-fed C57BL/6 mice (6 mice per group) for 6, 18, 32, or 54 weeks. The cells were transfected with DDX3 or miR-141 or siRNA to DDX3, and Western blots for autophagy markers were performed.</div></div><div><h3>Results</h3><div>The FFAs induced the DDX3 and miRNA-141 expression, while downregulating Sirt-1, beclin-1, Atg7, and LC3-II. Overexpression of DDX3 resulted in increased miRNA-141. Overexpression of DDX3 or miRNA-141 downregulated Sirt-1 expression and autophagy marker proteins, while these effects were reversed with siRNA to DDX3. The expression of both DDX3 and miRNA-141 was significantly increased, while autophagy markers were downregulated in CDAA-fed mice.</div></div><div><h3>Conclusions</h3><div>These results confirmed that FFA-induced DDX3 induced the expression of miRNA-141, which in turn targeted Sirt-1 and decreased autophagy.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101758"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778860","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}

引用次数: 0

Tumor-associated macrophages contribute to cholangiocarcinoma progression and chemoresistance through activation of ID1 肿瘤相关巨噬细胞通过激活 ID1 促进了胆管癌的发展和化疗耐药性。

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2024.101773

Yinghao Guo , Shuangda Miao , Yun Jin, Qi Li, Yihang Wang, Xiaoxiao Zhang, Jiangtao Li

{"title":"Tumor-associated macrophages contribute to cholangiocarcinoma progression and chemoresistance through activation of ID1","authors":"Yinghao Guo , Shuangda Miao , Yun Jin, Qi Li, Yihang Wang, Xiaoxiao Zhang, Jiangtao Li","doi":"10.1016/j.aohep.2024.101773","DOIUrl":"10.1016/j.aohep.2024.101773","url":null,"abstract":"<div><h3>Introduction and Objectives</h3><div>Tumor-associated macrophages (TAM) can influence both cancer growth and chemoresistance, but the specific mechanisms involved in these processes in cholangiocarcinoma (CCA) are unclear.</div></div><div><h3>Materials and Methods</h3><div>We explored the distribution of TAM in CCA samples by multiplex immunofluorescence staining and tested the effects of TAM on CCA in vitro and in vivo. We then investigated the mechanisms underlying these effects using the Luminex assay, RNA sequencing, western blotting, flow cytometry, and co-immunoprecipitation.</div></div><div><h3>Results</h3><div>The infiltration of TAM was strongly increased in the cholangiocarcinoma tumor microenvironment. Oncostain M (OSM) secreted by TAM increased the proliferation and chemotherapeutic resistance of CCA cells both in vitro and in vivo. The results of transcriptome sequencing analysis, Western blot analysis, and immunofluorescence staining confirmed that OSM can promote Yap nuclear translocation and its subsequent formation of complexes with SMADs to upregulate the expression of inhibitor of DNA binding 1 (ID1).</div></div><div><h3>Conclusions</h3><div>TAM promotes CCA progression and chemoresistance through activating OSM-Yap-ID1.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101773"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823857","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}

引用次数: 0

The role of inflammasomes in hepatocellular carcinoma: Mechanisms and therapeutic insights 炎性小体在肝细胞癌中的作用：机制和治疗见解。

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2024.101772

Valentina Arrè , Roberto Negro , Gianluigi Giannelli

{"title":"The role of inflammasomes in hepatocellular carcinoma: Mechanisms and therapeutic insights","authors":"Valentina Arrè , Roberto Negro , Gianluigi Giannelli","doi":"10.1016/j.aohep.2024.101772","DOIUrl":"10.1016/j.aohep.2024.101772","url":null,"abstract":"<div><div>Hepatocellular carcinoma is among the most frequent forms of primary liver cancer and develops within a context of chronic inflammation, frequently associated with a multitude of risk factors, including viral infections, metabolic dysfunction-associated fatty liver disease, metabolic dysfunction-associated steatohepatitis and liver fibrosis. The tumor microenvironment is crucial for the progression of HCC, as immune cells, tumor-associated fibroblasts and hepatic stellate cells interact to promote chronic inflammation and tumor spread. Inflammasomes, the multiprotein complexes that launch the innate immune response, emerge as important mediators in the pathogenesis of HCC. Among others, the inflammasome Nucleotide-binding oligomerization domain, Leucine rich Repeat (NLR) and Pyrin (NLRP) 3 (NLRP3), and absent in melanoma 2 (AIM2), exhibit a dual role in HCC background. It has been reported that they can exert oncosuppressive functions by triggering the inflammatory death of cancer cells. Vice versa, chronic activation contributes to the development of a pro-tumorigenic environment, thus supporting tumor growth. In addition, other inflammasomes such as Nucleotide-binding oligomerization domain, Leucine rich Repeat (NLR) and Pyrin (NLRP) 6 and 12 (NLRP6 and NLRP12, respectively) regulate HCC onset and progression, although more experimental evidence is required. This review focuses on the molecular mechanisms underpinning the inflammasome's contribution to the onset, progression and spread of HCC. Moreover, we will explore the potential therapeutic approaches currently under investigation, which aim to improve the efficacy and reduce the side effects of the treatments currently available. Targeting inflammasomes may be a promising therapeutic strategy for the treatment of HCC, offering new opportunities to improve patient prognosis.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101772"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863160","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}

引用次数: 0

MCM3 promotes hepatocellular carcinoma progression via Epithelial-mesenchymal Transition through AKT/Twist signaling pathway

IF 3.7 3区医学

Annals of hepatology Pub Date : 2025-01-01 DOI: 10.1016/j.aohep.2025.101785

Wei-Guo Tang , Jin-Feng Feng , Xian Li , Qi-Man Sun , Jin-Wu Hu , Xiao-Lu Ma , Yan-Yan Nie , Yang Xu , Jian Sun , Qi-Meng Chang

{"title":"MCM3 promotes hepatocellular carcinoma progression via Epithelial-mesenchymal Transition through AKT/Twist signaling pathway","authors":"Wei-Guo Tang , Jin-Feng Feng , Xian Li , Qi-Man Sun , Jin-Wu Hu , Xiao-Lu Ma , Yan-Yan Nie , Yang Xu , Jian Sun , Qi-Meng Chang","doi":"10.1016/j.aohep.2025.101785","DOIUrl":"10.1016/j.aohep.2025.101785","url":null,"abstract":"<div><h3>Introduction and Objectives</h3><div>Hepatocellular carcinoma (HCC), a leading cause of cancer fatalities, challenges clinicians with high recurrence and metastasis rates, urging the need for novel prognostic markers and therapeutic avenues. Minichromosome maintenance complex component 3 (MCM3) has been implicated in various cancers, but its role in HCC is not well-characterized.</div></div><div><h3>Materials and Methods</h3><div>We investigated MCM3 expression in HCC through cell line and patient sample analyses, functional assays to determine its effect on cellular behaviors, and signal pathway exploration.</div></div><div><h3>Results</h3><div>Elevated MCM3 expression was identified in both HCC cell lines and patient tissues, correlating with microvascular invasion, advanced cancer stage, and reduced survival. Functionally, MCM3 fueled HCC cellular proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and expedited tumor growth in vivo. Mechanistically, MCM3 was found to potentiate EMT by upregulating Twist via the AKT signaling pathway.</div></div><div><h3>Conclusions</h3><div>MCM3 emerges as an oncogenic influencer in HCC, driving disease progression through the AKT/Twist axis. Its expression patterns hold prognostic value, and targeting MCM3 may offer a novel therapeutic strategy for HCC.</div></div>","PeriodicalId":7979,"journal":{"name":"Annals of hepatology","volume":"30 1","pages":"Article 101785"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466557","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}

引用次数: 0