CLINICAL AND MOLECULAR HEPATOLOGY (CLIN MOL HEPATOL) 是一本国际性的、同行评审的、开放获取的期刊，每季度以英文出版。 CLIN MOL HEPATOL 旨在分享肝胆疾病的先进和最新知识、趋势和理解，为临床医生、转化研究人员和基础科学家之间的积极辩论和讨论提供一个广泛开放的学术论坛，并通过多学科合作改善公共卫生方法，特别是在资源有限的亚太地区，B 病毒感染和肝细胞癌的高发地区。此外，CLIN MOL HEPATOL 重点开展东亚、北亚、东南亚、中亚、南亚、西南亚、太平洋、非洲、中欧、东欧、中美洲和南美洲的肝胆疾病流行病学研究。

Clinical and Molecular Hepatology (CLIN MOL HEPATOL) is an international, peer-reviewed, open-access journal published quarterly in English. The journal aims to share advanced and up-to-date knowledge, trends, and understanding of hepatobiliary diseases, providing a broad academic forum for active debate and discussion among clinicians, translational researchers, and basic scientists. It seeks to improve public health approaches, particularly in resource-limited regions of the Asia-Pacific, where there is a high prevalence of hepatitis B virus infection and hepatocellular carcinoma. Furthermore, CLIN MOL HEPATOL focuses on epidemiological studies of hepatobiliary diseases in East Asia, North Asia, Southeast Asia, Central Asia, South Asia, Southwest Asia, the Pacific, Africa, Central Europe, Eastern Europe, Central America, and South America.

《Clinical and Molecular Hepatology》（CLIN MOL HEPATOL）是一本国际同行评审的开放获取期刊，每季度以英文出版。该期刊旨在分享肝胆疾病的最新研究成果和发展趋势，为临床医生、转化研究人员和基础科学家提供一个广泛的学术论坛，以促进积极的讨论和交流。期刊特别关注在资源有限的亚太地区，尤其是B型肝炎病毒感染和肝细胞癌高发地区的公共卫生改善。此外，《Clinical and Molecular Hepatology》还重点开展东亚、北亚、东南亚、中亚、南亚、西南亚、太平洋、非洲、中欧、东欧、中美洲和南美洲的肝胆疾病流行病学研究。

Clinical and Molecular Hepatology

“Metabolic dysfunction-associated fatty liver disease (MAFLD)” is the term suggested in 2020 to refer to fatty liver disease related to systemic metabolic dysregulation. The name change from nonalcoholic fatty liver disease (NAFLD) to MAFLD comes with a simple set of criteria to enable easy diagnosis at the bedside for the general medical community, including primary care physicians. Since the introduction of the term, there have been key areas in which the superiority of MAFLD over the traditional NAFLD terminology has been demonstrated, including for the risk of liver and extrahepatic mortality, disease associations, and for identifying high-risk individuals. Additionally, MAFLD has been adopted by a number of leading pan-national and national societies due to its concise diagnostic criterion, removal of the requirement to exclude concomitant liver diseases, and reduction in the stigma associated with this condition. The current article explores the differences between MAFLD and NAFLD diagnosis, areas of benefit, some potential limitations, and how the MAFLD terminology has opened up new fields of research.

Cameron Gofton

Yadhavan Upendran

Ming-Hua Zheng

Jacob George

Clin Mol Hepatol

MAFLD: How is it different from NAFLD?

MAFLD：它与NAFLD有何不同？

Evidence suggests that the gastrointestinal microbiome plays a significant role in the biology of metabolic dysfunction-associated steatotic liver disease (MASLD). However, it remains unclear whether disparities in the gut microbiome across intestinal tissular compartments between the sexes lead to MASLD pathogenesis.

Carlos Jose Pirola

Maria Silvina Landa

Mariano Schuman

Silvia Inés García

Adrian Salatino

Silvia Sookoian

Metabolic dysfunction-associated steatotic liver disease exhibits sex-specific microbial heterogeneity within intestinal compartments

代谢功能障碍相关脂肪性肝病表现出肠道分区内性别特异的微生物异质性

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver though a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

Chenyang Li

Chujun Cai

Chendong Wang

Xiaoping Chen

Bixiang Zhang

Zhao Huang

Gut microbiota-mediated gut-liver axis: a breakthrough point for understanding and treating liver cancer

肠道微生物介导的肠-肝轴：理解与治疗肝癌的突破点

Hiroyuki Suzuki

Tsubasa Tsutsumi

Machiko Kawaguchi

Keisuke Amano

Takumi Kawaguchi

Clinical and molecular hepatology

Changing from NAFLD to MASLD: Prevalence and progression of ASCVD risk are similar between NAFLD and MASLD in Asia.

从NAFLD到MASLD的转变：亚洲NAFLD与MASLD之间ASCVD风险的流行率和进展相似。

Metabolic dysfunction-associated fatty liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific proteinase 29 (USP29) plays pivotal roles in hepatic ischemia‒reperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression.

Sha Hu

Zhouxiang Wang

Kun Zhu

Hongjie Shi

Fang Qin

Tuo Zhang

Song Tian

Yanxiao Ji

Jianqing Zhang

Juanjuan Qin

Zhigang She

Xiaojing Zhang

Peng Zhang

Hongliang Li

USP29 alleviates the progression of MASLD by stabilizing ACSL5 through K48 deubiquitination

USP29通过K48去泛素化稳定ACSL5减轻MASLD的进展

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a global epidemic.MASLD has a strong genetic component, and a common missense variant (rs2642438) in the mitochondrial amidoxime-reducing component 1 (MARC1) gene confers protection against its onset and severity.However, there are contrasting results regarding the mechanisms entangling this protection. Methods:We downregulated MARC1 in primary human hepatocytes (PHH) using short interfering RNA (siRNA).Neutral lipid content was measured by Oil-Red O staining and fatty acid oxidation measured using radiolabeled tracers.RNA-seq and proteomic analysis using LC-MS were also performed.Additionally, we analyzed data from 239,075 participants from the UK Biobank.Results: Downregulation of MARC1 reduced neutral lipid content in PHH homozygous for the wild type (p.A165, risk) but not for the mutant (p.T165, protective) protein.Experimental results demonstrated that this reduction was mediated by an increased fatty acid utilization by beta-oxidation.Consistently, 3-hydroxybutyrate levels, a by-product of β-oxidation, were higher in carriers of the rs2642438 minor allele from the UK Biobank indicating higher βoxidation in these individuals.Moreover, downregulation of MARC1 p.A165 variant resulted in a more favorable phenotype by reducing ferroptosis and reactive oxygen species levels.Conclusions: MARC1 downregulation in carriers of the risk allele results in lower hepatocyte neutral lipids content due to higher β-oxidation, and upregulates beneficial pathways for cell survival.

Ester Ciociola

Tanmoy Dutta

Kavitha Sasidharan

Lohitesh Kovooru

Francesca R. Noto

Grazia Pennisi

Salvatore Petta

Angela Mirarchi

Samantha Maurotti

Bernardette Scopacasa

Luca Tirinato

Patrizio Candeloro

Marcus Henricsson

Daniel Lindén

Oveis Jamialahmadi

Arturo Pujia

Rosellina M. Mancina

Stefano Romeo

MARC1 downregulation reduces hepatocyte lipid content by increasing beta-oxidation

MARC1下调通过增加β-氧化减少肝细胞脂质含量

Yao-Chun Hsu

Chi-Yi Chen

Jaw-Town Lin

Expanding Treatment Eligibility for Chronic Hepatitis B: Balancing Benefits, Limitations, and Healthcare Access

扩大慢性乙型肝炎治疗资格：平衡效益、局限性与医疗可及性

Jing Zeng

Jian-Gao Fan

A leap in the dark: Bariatric surgery for treatment of metabolic dysfunction-associated steatotic liver disease related cirrhosis

黑暗中的跃进：代谢功能障碍相关脂肪性肝病相关肝硬化的减重手术治疗

Hai Xu

Yong Zhou

Huikun Wu

Comment on: Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma

评论：代谢功能障碍相关脂肪性肝病的演变及其与肝细胞癌风险的关联

Chunlong Liu

Jiangtao Yu

Global Inequality in the Burden of Hepatitis B From 1990 to 2021: Findings From the Global Burden of Disease Study 2021

1990年至2021年全球乙型肝炎负担的不平等性：2021年全球疾病负担研究结果

Abbreviation	Clin Mol Hepatol
Journal Impact	13.81
Quartiles(Global)	GASTROENTEROLOGY & HEPATOLOGY(Q1)

ISSN	2287-2728, 2287-285X
h-index	56

Publication Information	Publisher: Korean Association for the Study of the Liver，Publishing cycle: ，Journal Type: journal，Open Access Journals: Yes
Basic data	Year of publication: 2012，Proportion of original research papers: 60.00%，Self Citation Rate:18.60%， Gold OA Rate: 99.41%
Journal Fees	$Details
Average review cycle	网友分享经验：10 Weeks

Clinical and Molecular Hepatology

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