Clinical and Molecular Hepatology

HKDC1-Mediated Polyamine Rewiring Drives Lenvatinib Resistance and Immune Escape in Hepatocellular Carcinoma: Shiping Chen, Biao Wang, Yang Zhang, Bing Quan, Yujie Shao, Guiqi Zhu, Jialiang Cai, Peiling Zhang, Lina Song, Jinglei Wan, Yi Yang, Junxian Du, Yufan Cai, Zhi Dai; Received November 9, 2025 Accepted March 4, 2026 Published online March 11, 2026; DOI: https://doi.org/10.3350/cmh.2025.1269 [Accepted]

Abstract
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Background/Aims
Lenvatinib resistance and immune exclusion limit outcomes in HCC. We hypothesized that metabolic rewiring orchestrates resistance to lenvatinib and PD-1 blockade.
Methods
We established LS/LR HCC models and employed multi-omics (proteomics/RNA-seq), ChIP, luciferase, and RIP assays to map HKDC1 regulation. Tumor immunity was profiled by scRNA-seq, mIHC, and flow cytometry. SPD + lenvatinib efficacy was tested in cell lines, patient-derived organoids/xenografts. Tested therapy effect in an immunocompetent hydrodynamic HCC model with hepatocyte-specific Hkdc1 deletion; and analyzed a postoperative cohort (n = 40) treated with lenvatinib + PD-1.
Results
HKDC1, upregulated in LR HCC, was transcriptionally activated by USF1 and promoted SMS-mediated polyamine rewiring. This impaired CD8⁺ T-cell metabolism, reversible by HKDC1 knockdown or spermidine (SPD). SPD synergized with lenvatinib, triggering autophagy and suppressing tumor growth in vitro and in vivo. High HKDC1 predicted poor response and survival in patients receiving lenvatinib + aPD-1.
Conclusions
A USF1/HKDC1/SMS axis couples polyamine metabolism to immune dysfunction and lenvatinib resistance. HKDC1 is a predictive biomarker and therapeutic node and support polyamine-axis modulation to sensitize HCC to lenvatinib plus PD-1 therapy.

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Targeting ER lipid raft-associated 1 reveals a coordinated cholesterol-dependent vulnerability in hepatocellular carcinoma: Yiming Zhang, Yushan Hou, Xinxin Wang, Kaikun Xu, Pei Jiang, Siqi Wang, Huimin Kang, Hu Zhang, Jingzhuo Jin, Xiaofen Huang, Zifeng Liu, Songpeng Yang, Jiaqi Liu, Lingqiang Zhang, Fuchu He, Chunyan Tian, Aihua Sun; Clin Mol Hepatol 2026;32(2):866-883.
Published online February 11, 2026; DOI: https://doi.org/10.3350/cmh.2025.1157

Background/Aims
Dysregulated cholesterol metabolism is a hallmark of hepatocellular carcinoma (HCC) that drives tumor initiation and progression. However, clinical targeting of cholesterol metabolism has yielded limited benefits due to stringent feedback in tumor cells. Identifying a central mediator capable of restoring cholesterol homeostasis within the cell’s intrinsically fine-tuned regulatory framework is urgently needed.
Methods
We integrated a proteomic dataset from patients with cholesterol-dysregulated HCC into a global cholesterol metabolic regulatory network to identify potential therapeutic targets for disrupted cholesterol homeostasis. The prognostic significance of the candidate targets was further validated in an independent cohort through immunohistochemistry. Functional and mechanistic studies were conducted in vitro using HCC cell lines and in vivo using mouse models. The pharmacological efficacy of the candidate agent was evaluated in both subcutaneous and orthotopic HCC mouse models.
Results
ER lipid raft-associated 1 (ERLIN1), a pivotal regulator of cholesterol metabolism reprogramming, was identified as an independent favorable prognostic indicator in HCC. ERLIN1 constrains HCC progression both in vitro and in vivo by stabilizing the INSIG1–SCAP–SREBP2 axis and maintaining the metabolic balance of intracellular cholesterol. Under hypoxia, impaired factor-inhibiting hypoxia-1-dependent hydroxylation of ASB11 at asparagine residues 90 and 92 enhances ASB11-mediated ERLIN1 degradation. Pharmacological targeting of this axis using zoledronic acid (ZoA) attenuated HCC progression by weakening the ASB11–ERLIN1 interaction and restoring cholesterol homeostasis.
Conclusions
ERLIN1 represents a druggable metabolic vulnerability in cholesterol-dysregulated HCC. Targeting the ASB11–ERLIN1 axis with the clinically approved ZoA reestablishes cholesterol homeostasis and offers a promising therapeutic strategy to overcome the current limitations of cholesterol-targeted HCC therapies.

1,437 View
171 Download

Letter to the editor on “Role of amino acids in the regulation of hepatic gluconeogenesis and lipogenesis in metabolic dysfunctionassociated steatotic liver disease”: Xinyi Cai, Lu Zhang, Tuo Li; Clin Mol Hepatol 2026;32(2):e136-e138.
Published online July 21, 2025; DOI: https://doi.org/10.3350/cmh.2025.0731

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3,748 View
57 Download

Correspondence to letter to the editor on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”: Tomoko Aoki, Naoshi Nishida, Masatoshi Kudo; Clin Mol Hepatol 2026;32(2):e241-e243.
Published online July 14, 2025; DOI: https://doi.org/10.3350/cmh.2025.0760

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2,662 View
26 Download

Reply to correspondence on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”: Eun Ji Jang, Pil Soo Sung; Clin Mol Hepatol 2026;32(1):e115-e116.
Published online May 13, 2025; DOI: https://doi.org/10.3350/cmh.2025.0498

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4,865 View
32 Download

Correspondence to editorial on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”: Tomoko Aoki, Naoshi Nishida, Masatoshi Kudo; Clin Mol Hepatol 2026;32(1):e79-e82.
Published online April 28, 2025; DOI: https://doi.org/10.3350/cmh.2025.0435

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Reply to correspondence on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”
Eun Ji Jang, Pil Soo Sung
Clinical and Molecular Hepatology.2026; 32(1): e115. CrossRef
Fluorine-18 Fluorodeoxyglucose Positron Emission Tomography: A Potential Imaging Biomarker for Predicting Response to Combination Immunotherapy in Hepatocellular Carcinoma
Masatoshi Kudo
Liver Cancer.2025; 14(5): 511. CrossRef

5,575 View
38 Download
Crossref

A novel link between tumor cell metabolism and patient prognosis: Editorial on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”: Eun Ji Jang, Pil Soo Sung; Clin Mol Hepatol 2026;32(1):420-422.
Published online April 16, 2025; DOI: https://doi.org/10.3350/cmh.2025.0395

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Correspondence to editorial on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”
Tomoko Aoki, Naoshi Nishida, Masatoshi Kudo
Clinical and Molecular Hepatology.2026; 32(1): e79. CrossRef
Reply to correspondence on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”
Eun Ji Jang, Pil Soo Sung
Clinical and Molecular Hepatology.2026; 32(1): e115. CrossRef
Clinical Prediction of Glycolysis-Driven Molecular Subclass of Hepatocellular Carcinoma without Transcriptomic Profiling
Tomoko Aoki, Masatoshi Kudo, Satoshi Ogiso, Genki Okumura, Megumi Hoshino, Yuka Nakamura, Ryo Morisue, Shohei Koyama, Naoshi Nishida, Kohei Hanaoka, Kazuko Sakai, Yutaka Kurebayashi, Masakatsu Tsurusaki, Masahiro Morita, Atsushi Takebe, Takaaki Murase, Ke
Liver Cancer.2026; : 1. CrossRef
Fluorine-18 Fluorodeoxyglucose Positron Emission Tomography: A Potential Imaging Biomarker for Predicting Response to Combination Immunotherapy in Hepatocellular Carcinoma
Masatoshi Kudo
Liver Cancer.2025; 14(5): 511. CrossRef

3,243 View
36 Download
Crossref

Regulation of hepatitis B virus cccDNA by metabolic pathways: Editorial on “GDH1-dependent α-ketoglutarate promotes HBV transcription by modulating histone methylations on the cccDNA minichromosome”: Hyeong-Jin Cho, Sung-Gyoo Park; Clin Mol Hepatol 2026;32(1):381-384.
Published online March 12, 2025; DOI: https://doi.org/10.3350/cmh.2025.0255

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Establishment and evaluation of an immortalized dzo kidney cell line
Wenkai Liu, Cong Xu, Jiamin Wang, Na Sun, Zhongren Ma, Jin Zhao, Jianguo Chen, You Li, Zilin Qiao
Scientific Reports.2025;[Epub] CrossRef

5,633 View
122 Download
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Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway: Tomoko Aoki, Naoshi Nishida, Yutaka Kurebayashi, Kazuko Sakai, Naoto Fujiwara, Masakatsu Tsurusaki, Kohei Hanaoka, Masahiro Morita, Hirokazu Chishina, Masahiro Takita, Satoru Hagiwara, Hiroshi Ida, Kazuomi Ueshima, Yasunori Minami, Atsushi Takebe, Takaaki Murase, Keiko Kamei, Takuya Nakai, Ippei Matsumoto, Kazuto Nishio, Masatoshi Kudo; Clin Mol Hepatol 2025;31(3):981-1002.
Published online March 11, 2025; DOI: https://doi.org/10.3350/cmh.2024.1088

Background/Aims
Previously, we advocated the importance of classifying hepatocellular carcinoma (HCC) based on physiological functions. This study aims to classify HCC by focusing on liver-intrinsic metabolism and glycolytic pathway in cancer cells.
Methods
Comprehensive RNA/DNA sequencing, immunohistochemistry, and radiological evaluations were performed on HCC tissues from the training cohort (n=136) and validated in 916 public samples. HCC was classified using hierarchical clustering and compared with previous molecular, histopathological, and hemodynamic classifications.
Results
Liver-specific metabolism and glycolysis are mutually exclusive and were divided into two major subclasses: The “rich metabolism” subclass (60.3%) is characterized by enhanced bile acid and fatty acid metabolism, wellto-moderate differentiation, microtrabecular or pseudoglandular pattern, and homogeneous arterial-phase hyperenhancement (APHE), corresponding to Hoshida S3 with favorable prognosis. In IL6-JAK-STAT3-high (25.0%) conditions, upregulated ALB expression, enhanced gluconeogenesis and urea cycle activity, and an inflammatorymicroenvironment are observed. Conversely, the Wnt/β-catenin-high environment (19.9%) features elevated GLUL, APOB and CYP3A4 expression, frequent CTNNB1 (D32–S37) mutations, and an immune-desert/excluded phenotype. The “glycolysis” subclass (39.7%), characterized by histopathological dedifferentiation and downregulated liver-specific metabolism, encompasses subclasses with PI3K/mTOR (20.6%) and NOTCH/TGF-β (19.1%) signaling. These often exhibit TP53 mutations, macrotrabecular massive or compact patterns, inhomogeneous/rim-APHE, and high expression of hypoxia-inducible factors and glucose transporters, corresponding to Hoshida S1/2 with poor prognosis.
Conclusions
The loss of liver-specific metabolism correlates with morphological dedifferentiation, indicating cellular dedifferentiation may exhibit both physiological and pathological duality. Key signaling pathways involved in the maturation process from fetal to adult liver and zonation program may play a critical role in defining HCC diversity.

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Molecular stratification of hepatocellular carcinoma by metabolic-signaling pathways guides precision immunotherapy and TACE therapy
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Zonation, Zonation, Zonation: The Real Estate of the Liver
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Clinical and Molecular Hepatology.2026; 32(2): e241. CrossRef
Critical flaws in the molecular classification of HCC based on metabolic zonation: Letter to the editor on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway”
Yongzhi Xie, Xiangyu Zhu, Qi Liang
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Clinical applications of immunogenomics in hepatocellular carcinoma
James K. Carter, Daniel C. Cameron, Augusto Villanueva
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Unveiling the Intricate Dance: Signaling Pathways in Liver Cancer Metabolism and Immunity
Yichi Xu, Bo Wen, Dai Zhang, Fangxin Tang, Shu Liu
Current Oncology Reports.2026;[Epub] CrossRef
Clinical Prediction of Glycolysis-Driven Molecular Subclass of Hepatocellular Carcinoma without Transcriptomic Profiling
Tomoko Aoki, Masatoshi Kudo, Satoshi Ogiso, Genki Okumura, Megumi Hoshino, Yuka Nakamura, Ryo Morisue, Shohei Koyama, Naoshi Nishida, Kohei Hanaoka, Kazuko Sakai, Yutaka Kurebayashi, Masakatsu Tsurusaki, Masahiro Morita, Atsushi Takebe, Takaaki Murase, Ke
Liver Cancer.2026; : 1. CrossRef
Fluorine-18 Fluorodeoxyglucose Positron Emission Tomography: A Potential Imaging Biomarker for Predicting Response to Combination Immunotherapy in Hepatocellular Carcinoma
Masatoshi Kudo
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14,132 View
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16 Web of Science
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Steatotic liver disease

Reply to correspondence 1 on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”: Yoon-su Ha, Won Kim, Seung-Jin Kim; Clin Mol Hepatol 2025;31(2):e226-e227.
Published online February 13, 2025; DOI: https://doi.org/10.3350/cmh.2025.0128

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6,456 View
43 Download

Interventions targeting the gut-liver axis: A potential treatment strategy for metabolic dysfunction-associated steatotic liver disease: Pingping Jin, Xinyi Lu, Daozhen Chen, Yu Chen; Clin Mol Hepatol 2025;31(3):1100-1102.
Published online February 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.1090

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Probiotic-Derived Strain-Specific Metabolites Ameliorate Metabolic Dysfunction–Associated Steatotic Liver Disease through Modulation of the Gut-Liver Axis
Sang Jun Yoon, Jieun Choi, Sung-Min Won, Jeong Seok Yu, Hee Young Kim, Hyun Chae Joung, In Gyu Park, Jung A Eom, Sang Hak Han, Do Yup Lee, Ki Tae Suk
Probiotics and Antimicrobial Proteins.2026; 18(3): 4353. CrossRef
Scutellaria baicalensis extract prevents metabolic dysfunction-associated steatotic liver disease by modulating the gut-liver axis in high-fat diet mice
Liting Ma, Yizhu Wang, Tao Ren, Lijia Pan, Xinze Li, Shen Wang, Dihao Li, Meiyu Zhang, Fangtong Li, Fei Zheng, Hao Yue
Phytochemistry.2026; 243: 114720. CrossRef
Hypertension and Long-Term Adverse Clinical Outcomes in MASLD: Sensitivity Analyses for Unmeasured or Uncontrolled Confounding
Guiying Gao, Xiuhong Wang, Ruizhe Huang, Jing Cao
Journal of Hepatology.2026;[Epub] CrossRef
Extracellular Vesicles: Orchestrators of Intrahepatic and Systemic Crosstalk in Metabolic Dysfunction-Associated Steatotic Liver Disease
Yu Lei, Mei Liu, Xiang Tao
Pharmaceutics.2026; 18(1): 116. CrossRef
Hydrogel-Based Therapeutic Strategies for Post-Cholecystectomy NAFLD: Targeting Bile Acid Signaling, Gut Microbiota, Inflammation, and Hepatic Fibrosis
Georgiana-Andreea Marinescu, Alexandra-Daniela Rotaru-Zavaleanu, Emil-Tiberius Trasca, Elena-Irina Caluianu, Oana Taisescu, Andrei Gresita, Madalina Iuliana Musat, Dumitru Radulescu, Razvan Mercut, Citto-Iulian Taisescu
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Expert Review of Gastroenterology & Hepatology.2025; 19(12): 1329. CrossRef

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Steatotic liver disease

Bridging the gap: The GOLM1-OPN-ABCG5 axis in MASH and gallstone disease: Editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”: Nahee Hwang, Sungsoon Fang; Clin Mol Hepatol 2025;31(2):631-634.
Published online February 3, 2025; DOI: https://doi.org/10.3350/cmh.2025.0066

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Biomimetic Nanomedicine for Senescence‐Modulated Immune Activation Enhances Immunotherapy Efficacy in Hepatocellular Carcinoma
Shiji Fang, Liyun Zheng, Bin Lin, Jiale Chen, Dehai Hou, Yiming Ding, Mengzhu Han, Pan Qin, Mengyuan Wang, Xiaoju Guo, Yeyu Zhang, Gaofeng Shu, Fazong Wu, Jianfei Tu, Minjiang Chen, Zhongwei Zhao, Zhuang Liu, Jiansong Ji
Advanced Science.2026;[Epub] CrossRef
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Mengyan Du, Lvwang Ye, Cong Wang, Ting Jiang, Fang Liu
Journal of Functional Foods.2026; 139: 107194. CrossRef
GOLM1 and bile acid synthesis: Correspondence to editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yi-Tong Li, Wei-Qing Shao, Zhen-Mei Chen, Jing Lin, Jin-Hong Chen
Clinical and Molecular Hepatology.2025; 31(2): e189. CrossRef
Reply to correspondence 2 on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Nahee Hwang, Sungsoon Fang
Clinical and Molecular Hepatology.2025; 31(2): e228. CrossRef
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Yuezhan Shan, Hongyu Chu, Sheyu Ye, Guofeng Ji, Jiayi Zhao, Xinghui Si, Yumin Zhong, Youmao Tao, Jingwei Shi, Xuedong Fang
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A demethylation chloroisosulochrin and a chromone metabolite from the endophytic fungus Penicilium sp.
Ke-Liang Chen, Xue Wang, Yang Liu, Yun-Bao Liu
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Steatotic liver disease

Correspondence to editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”: Yi-Tong Li, Wei-Qing Shao, Zhen-Mei Chen, Jing Lin, Jin-Hong Chen; Clin Mol Hepatol 2025;31(2):e186-e188.
Published online January 24, 2025; DOI: https://doi.org/10.3350/cmh.2025.0079

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Citations to this article as recorded by

Reply to correspondence 1 on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yoon-su Ha, Won Kim, Seung-Jin Kim
Clinical and Molecular Hepatology.2025; 31(2): e226. CrossRef

6,388 View
42 Download
1 Web of Science
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Steatotic liver disease

Unraveling the role of GOLM1-OPN-ABCG5 axis in MASH: Editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”: Yoon-su Ha, Won Kim, Seung-Jin Kim; Clin Mol Hepatol 2025;31(2):628-630.
Published online January 16, 2025; DOI: https://doi.org/10.3350/cmh.2025.0036

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Citations to this article as recorded by

Reply to correspondence 1 on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yoon-su Ha, Won Kim, Seung-Jin Kim
Clinical and Molecular Hepatology.2025; 31(2): e226. CrossRef
Correspondence to editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yi-Tong Li, Wei-Qing Shao, Zhen-Mei Chen, Jing Lin, Jin-Hong Chen
Clinical and Molecular Hepatology.2025; 31(2): e186. CrossRef

7,271 View
72 Download
2 Web of Science
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Steatotic liver disease

GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in metabolic dysfunction-associated steatohepatitis livers: Yi-Tong Li, Wei-Qing Shao, Zhen-Mei Chen, Xiao-Chen Ma, Chen-He Yi, Bao-Rui Tao, Bo Zhang, Yue Ma, Guo Zhang, Rui Zhang, Yan Geng, Jing Lin, Jin-Hong Chen; Clin Mol Hepatol 2025;31(2):409-425.
Published online December 10, 2024; DOI: https://doi.org/10.3350/cmh.2024.0657

Background/Aims
Metabolic dysfunction-associated steatohepatitis (MASH) is a significant risk factor for gallstone formation, but mechanisms underlying MASH-related gallstone formation remain unclear. Golgi membrane protein 1 (GOLM1) participates in hepatic cholesterol metabolism and is upregulated in MASH. Here, we aimed to explore the role of GOLM1 in MASH-related gallstone formation.
Methods
The UK Biobank cohort was used for etiological analysis. GOLM1 knockout (GOLM1^-/-) and wild-type (WT) mice were fed with a high-fat diet (HFD). Livers were excised for histology and immunohistochemistry analysis. Gallbladders were collected to calculate incidence of cholesterol gallstones (CGSs). Biles were collected for biliary lipid analysis. HepG2 cells were used to explore underlying mechanisms. Human liver samples were used for clinical validation.
Results
MASH patients had a greater risk of cholelithiasis. All HFD-fed mice developed MASH, and the incidence of gallstones was 16.7% and 75.0% in GOLM1^-/- and WT mice, respectively. GOLM1^-/- decreased biliary cholesterol concentration and output. In vivo and in vitro assays confirmed that GOLM1 facilitated cholesterol efflux through upregulating ATP binding cassette transporter subfamily G member 5 (ABCG5). Mechanistically, GOLM1 translocated into nucleus to promote osteopontin (OPN) transcription, thus stimulating ABCG5-mediated cholesterol efflux. Moreover, GOLM1 was upregulated by interleukin-1β (IL-1β) in a dose-dependent manner. Finally, we confirmed that IL-1β, GOLM1, OPN, and ABCG5 were enhanced in livers of MASH patients with CGSs.
Conclusions
In MASH livers, upregulation of GOLM1 by IL-1β increases ABCG5-mediated cholesterol efflux in an OPN-dependent manner, promoting CGS formation. GOLM1 has the potential to be a molecular hub interconnecting MASH and CGSs.

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Methylation changes of gallbladder DNA during the formation of gallstones
Hongyu Xu, Jinlong Hu, Jinshan Liu, Rui Wang, Junbin Peng, Peilin Liu, Jiaming Yao, Baoqiang Cao
Epigenomics.2026; 18(1): 55. CrossRef
Biliary elimination of cholesterol can be modulated by hepatocyte mitochondrial Aquaporin-8 in mice
María Celeste Capitani, Alejo M. Capiglioni, Raúl A. Marinelli, Julieta Marrone
Scientific Reports.2026;[Epub] CrossRef
Association of arm circumference with the prevalence of gallstones in United States adults: a retrospective analysis on US National Health and Nutrition Examination Survey
Jianjun Wang, Xi Chen, Wei He, Xintao Zeng, Pei Yang, Jianping Gong, Decai Wang
Frontiers in Medicine.2025;[Epub] CrossRef
Reply to correspondence 2 on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Nahee Hwang, Sungsoon Fang
Clinical and Molecular Hepatology.2025; 31(2): e228. CrossRef
Unraveling the role of GOLM1-OPN-ABCG5 axis in MASH: Editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yoon-su Ha, Won Kim, Seung-Jin Kim
Clinical and Molecular Hepatology.2025; 31(2): 628. CrossRef
Bridging the gap: The GOLM1-OPN-ABCG5 axis in MASH and gallstone disease: Editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Nahee Hwang, Sungsoon Fang
Clinical and Molecular Hepatology.2025; 31(2): 631. CrossRef
Correspondence to editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yi-Tong Li, Wei-Qing Shao, Zhen-Mei Chen, Jing Lin, Jin-Hong Chen
Clinical and Molecular Hepatology.2025; 31(2): e186. CrossRef
GOLM1 and bile acid synthesis: Correspondence to editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yi-Tong Li, Wei-Qing Shao, Zhen-Mei Chen, Jing Lin, Jin-Hong Chen
Clinical and Molecular Hepatology.2025; 31(2): e189. CrossRef
Reply to correspondence 1 on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yoon-su Ha, Won Kim, Seung-Jin Kim
Clinical and Molecular Hepatology.2025; 31(2): e226. CrossRef
Pharmacological effects and prospects of traditional Chinese medicine and its bioactive components in the prevention and treatment of urolithiasis and cholelithiasis
Dan Jiang, Xiaofeng Zhou, Xiaolong Lu
Letters in Drug Design & Discovery.2025; 22(12): 100274. CrossRef

11,031 View
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11 Web of Science
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Steatotic liver disease

USP29 alleviates the progression of MASLD by stabilizing ACSL5 through K48 deubiquitination: 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; Clin Mol Hepatol 2025;31(1):147-165.
Published online October 2, 2024; DOI: https://doi.org/10.3350/cmh.2024.0478

Background/Aims
Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion 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.
Methods
USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes.
Results
USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5.
Conclusions
USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

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Cell Death & Differentiation.2026; 33(3): 525. CrossRef
Deubiquitinases in liver diseases: from mechanisms to targeted therapy
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Steatotic liver disease

Evaluating the therapeutic efficacy of NAD supplementation in management of metabolic dysfunction-associated steatotic liver disease: Key considerations: Xinyi Lu, Rui Yang, Yu Chen, Daozhen Chen; Clin Mol Hepatol 2024;30(3):582-584.
Published online December 29, 2023; DOI: https://doi.org/10.3350/cmh.2023.0555

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Citations

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β-Nicotinamide Mononucleotide protects against endotoxemia-induced myocardial injury through Sirt5-dependent desuccinylation of succinate dehydrogenase
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Viral hepatitis

The impact of pegylated interferon and ribavirin combination treatment on lipid metabolism and insulin resistance in chronic hepatitis C patients: Hee Jae Jung, Young Seok Kim, Sang Gyune Kim, Yun Nah Lee, Soung Won Jeong, Jae Young Jang, Sae Hwan Lee, Hong Soo Kim, Boo Sung Kim; Clin Mol Hepatol 2014;20(1):38-46.
Published online March 26, 2014; DOI: https://doi.org/10.3350/cmh.2014.20.1.38

Abstract
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Background/Aims

Lipid profile and insulin resistance (IR) are associated with hepatitis C virus (HCV) and may predict the chronic hepatitis C (CHC) treatment response. The aim of this study was to determine the association between CHC treatment response and lipid profile and IR change during treatment.

Methods

In total, 203 CHC patients were reviewed retrospectively between January 2005 and December 2011 at Soon Chun Hyang University Hospital. The lipid profile, homeostasis model for assessment (HOMA) of IR (HOMA-IR), and HOMA of β cells (HOMA-β) were evaluated before interferon plus ribavirin therapy (BTx), at the end of treatment (DTx), and 24 weeks after the end of treatment (ATx).

Results

A sustained virologic response (SVR) was achieved by 81% of all patients (49/60), 60% (n=36) of whom possessed genotype 1, with the remainder being non-genotype-1 (40%, n=24). Apart from age, which was significantly higher in the non-SVR group (SVR, 48.0±11.2 years, mean±SD; non-SVR, 56.6±9.9 years; P<0.01), there were no significant differences in the baseline characteristics between the SVR and non-SVR groups. In the SVR group, low density lipoprotein-cholesterol (LDL-C) had significantly changed at DTx and ATx compared to BTx. In addition, HOMA-IR and HOMA-β were significantly changed at DTx in the SVR group. Among those with a high baseline insulin resistance (HOMA-IR >2.5), HOMA-IR was significantly changed at DTx in the SVR group.

Conclusions

LDL-C appears to be associated with HCV treatment in SVR patients. Furthermore, eradication of HCV may improve whole-body IR and insulin hypersecretion, as well as high baseline insulin resistance (HOMA-IR >2.5).

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