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"Fatty acid"

Original Article

MTARC1 p.A165 ablation reduces hepatocellular carcinoma aggressiveness in vitro and in vivo
Lohitesh Kovooru, Jingjing Zhang, Francesco Giuseppe Monni, Tanmoy Dutta, Xiangdong Gongye, Bernice Asiedu, Patrizia Infelise, Emelie Barreby, Oveis Jamialahmadi, Margit Mahlapuu, Rosellina M. Mancina, Stefano Romeo
Clin Mol Hepatol 2026;32(2):829-842.
Published online February 5, 2026
DOI: https://doi.org/10.3350/cmh.2025.1261
Background/Aims
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide and is driven by metabolic reprogramming that supports tumor growth and progression. A common missense genetic variant (rs2642438, p.A165T) in mitochondrial amidoxime reducing component 1 (MTARC1), identified as protective against liver disease, has been recently associated with lower prevalence of steatosis, cirrhosis, and HCC. However, the mechanistic role of MTARC1 in HCC is unclear. Therefore, we sought to decipher the role of MTARC1 in HCC.
Methods
We investigated the role of MTARC1 in HCC by performing siRNA-mediated knockdown across human immortalized HCC cell lines (Hep3B2, HuH7, HepG2 and HepaRG) homozygous for the risk allele (p.A165) and by generating stable CRISPR-Cas9 knockout (KO) models. Next, we assessed the effect of MTARC1 loss on cell proliferation, migration, lipid metabolism, and fatty acid oxidation in vitro, as well as tumor aggressiveness in a subcutaneous xenograft mouse model. Additionally, we performed global proteomics in both in vitro and xenograft models.
Results
Transient knockdown of MTARC1 p.A165 reduced proliferation in HCC cell lines. CRISPR-Cas9-mediated stable MTARC1 p.A165 KO in Hep3B2 cells led to decreased neutral lipid intracellular accumulation, enhanced β-oxidation and reduced cell migration. An MTARC1 KO xenograft model had reduced tumor volume. Proteomic analyses of both in vitro HCC cells and xenograft tumors revealed inhibition of oncogenic pathways and activation of anti-proliferative proteins.
Conclusions
Downregulation of MTARC1 p.A165 inhibits lipid accumulation, dampens tumor-promoting pathways and restricts tumor growth, highlighting MTARC1 as a promising therapeutic target for HCC.

Citations

Citations to this article as recorded by  Crossref logo
  • Mapping the genomic landscape of MASLD: A framework for molecular subtyping and precision hepatology
    Carlos José Pirola, Silvia Sookoian
    Med.2026; 7(6): 101131.     CrossRef
  • 2,488 View
  • 177 Download
  • 1 Web of Science
  • Crossref

Correspondence

Correspondence to editorial 2 on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
Dongqin Yang, Yuli Lin, Chunhua Song, Ming Guan
Clin Mol Hepatol 2026;32(3):e342-e345.
Published online September 29, 2025
DOI: https://doi.org/10.3350/cmh.2025.1100
  • 1,690 View
  • 78 Download

Editorials

ASB3 degrades the gateway to β-oxidation: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
Ho Jae Ryu, Ji Su Han, Ja Hyun Koo
Clin Mol Hepatol 2026;32(3):1379-1382.
Published online September 23, 2025
DOI: https://doi.org/10.3350/cmh.2025.1021

Citations

Citations to this article as recorded by  Crossref logo
  • TREM1-mediated macrophage activation drives voriconazole-induced hepatic steatosis: Diagnostic and therapeutic implications
    Jing Liu, Mingxia Deng, Xiaoying He, Jing Ma, Li Zhang, Xi Yang, Jinyao Dai, Shaohua Dong, Yichun Zhang, Zhijuan Zhang, Shuaibing Ying, Haoyang Hu, Lushun Jiang, Yujing Wang, Yunqing Qiu, Yan Lou
    Journal of Pharmaceutical Analysis.2026; 16(6): 101540.     CrossRef
  • Correspondence to editorial 2 on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
    Dongqin Yang, Yuli Lin, Chunhua Song, Ming Guan
    Clinical and Molecular Hepatology.2026; 32(3): e342.     CrossRef
  • 2,139 View
  • 163 Download
  • 1 Web of Science
  • Crossref
Targeting the ASB3-CPT1A axis—a new player in combating metabolic dysfunction-associated steatotic liver disease: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyltransferase 1A”
Yueying Yang, Ying Yang, Yan Lu
Clin Mol Hepatol 2026;32(2):957-959.
Published online September 15, 2025
DOI: https://doi.org/10.3350/cmh.2025.1013

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial 1 on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
    Yuli Lin, Dongqin Yang, Zhihao Wu, Ming Guan, Chunhua Song
    Clinical and Molecular Hepatology.2026; 32(3): e339.     CrossRef
  • 2,503 View
  • 90 Download
  • 1 Web of Science
  • Crossref

Original Article

Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A
Yuli Lin, Wulei Hou, Mengxiao Ge, Zhihao Wu, Linlin Huang, Haoye Liu, Wenli Zhang, Xiyu Deng, Lanxin Wang, Ming Guan, Chunhua Song, Zuoyun Wang, Dongqin Yang
Clin Mol Hepatol 2025;31(4):1333-1354.
Published online August 8, 2025
DOI: https://doi.org/10.3350/cmh.2024.1041
Background/Aims
Excessive lipid accumulation in hepatocytes is a critical cause of metabolic dysfunction-associated steatotic liver disease (MASLD) progression. Ankyrin repeat and SOCS box protein 3 (ASB3) is an E3 ubiquitin ligase that mediates diverse disease processes; however, the direct substrates of ASB3 in lipid metabolism and its role in MASLD remain unexplored.
Methods
We generated ASB3 knockout mice fed a high-fat diet to induce MASLD. Oxygen consumption and fatty acid oxidation (FAO) were used to assess lipid metabolism. LC-MS/MS and IP were used to verify the ASB3 target protein. Correlation analysis was conducted on the cohort of MASLD patients vs. the control group.
Results
Loss of the ASB3 E3 ubiquitin ligase in hepatocytes strengthens mitochondrial FAO, thereby influencing energy consumption to decrease triglyceride storage and lipid accumulation. Quantitative lysine ubiquitination proteomics revealed that ASB3 directly mediated the ubiquitin levels at two sites (K180 and K639) in carnitine palmitoyl transferase 1A (CPT1A), a rate-limiting enzyme of FAO, to induce CPT1A degradation. Moreover, both constitutive and hepatocyte-specific ASB3 knockout enhance FAO and delay lipid accumulation, liver steatosis, and MASLD progression in a CPT1A-dependent manner. Hepatic ASB3 deficiency also delays fibrosis in MASLD. Analysis of public databases and liver tissue samples from MASLD patients revealed that ASB3 was highly expressed in MASLD patients and was negatively correlated with CPT1A.
Conclusions
Our study reveals the key roles of ASB3 in the development of MASLD and suggests a novel therapeutic potential for MASLD.

Citations

Citations to this article as recorded by  Crossref logo
  • Targeting the ASB3-CPT1A axis—a new player in combating metabolic dysfunction-associated steatotic liver disease: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver diseas
    Yueying Yang, Ying Yang, Yan Lu
    Clinical and Molecular Hepatology.2026; 32(2): 957.     CrossRef
  • The first genome-wide association study on pediatric obesity in Taiwan
    Hsin-Ru Wu, Ting-Yuan Liu, Chuan-Mu Chen, Fuu-Jen Tsai
    Journal of the Formosan Medical Association.2026;[Epub]     CrossRef
  • Correspondence to editorial 1 on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
    Yuli Lin, Dongqin Yang, Zhihao Wu, Ming Guan, Chunhua Song
    Clinical and Molecular Hepatology.2026; 32(3): e339.     CrossRef
  • Correspondence to editorial 2 on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
    Dongqin Yang, Yuli Lin, Chunhua Song, Ming Guan
    Clinical and Molecular Hepatology.2026; 32(3): e342.     CrossRef
  • ASB3 degrades the gateway to β-oxidation: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
    Ho Jae Ryu, Ji Su Han, Ja Hyun Koo
    Clinical and Molecular Hepatology.2026; 32(3): 1379.     CrossRef
  • A multi-herb botanical formula ameliorates diet-induced non-alcoholic fatty liver disease associated with microbiota-dependent metabolic remodeling in mice
    Xinrui Meng, Fan Wang, Ying Li, Yan Li, Meiping Zhang, Jing Cong
    Food Research International.2026; 243: 120383.     CrossRef
  • ASB3 limits adipocyte thermogenesis and energy expenditure through p62 ubiquitination
    Mengyu Shi, Haoye Liu, Zhihao Wu, Linlin Huang, Chunhua Song, Yuli Lin, Dongqin Yang
    Metabolism.2026; 184: 156756.     CrossRef
  • 7,460 View
  • 559 Download
  • 5 Web of Science
  • Crossref

Reply to Correspondence

Metabolic dysfunction-associated steatotic liver disease: On track to become the dominant etiology of hepatocellular carcinoma: Reply to correspondence on “Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta-oxidation”
Jian Xu, Wei Zhang, Guo Wu, Jingdong Li
Clin Mol Hepatol 2026;32(2):e257-e261.
Published online August 6, 2025
DOI: https://doi.org/10.3350/cmh.2025.0853
  • 4,237 View
  • 72 Download

Review

Role of amino acids in the regulation of hepatic gluconeogenesis and lipogenesis in metabolic dysfunctionassociated steatotic liver disease
Eiji Kakazu, Masaaki Mino, Tatsuya Kanto
Clin Mol Hepatol 2025;31(3):771-795.
Published online April 16, 2025
DOI: https://doi.org/10.3350/cmh.2025.0048
Metabolic dysfunction-associated steatotic liver disease (MASLD) and its relatively advanced form, metabolic dysfunction-associated steatohepatitis (MASH), are becoming increasingly prevalent worldwide, making their prevention and management an urgent global health priority. Central to their development are key metabolic defects, including abnormal concentrations of monosaccharides, fatty acids, and amino acids, but the complex relationships between these substances within the hepatic microenvironment remain only partially understood. Dysregulated glucose metabolism and selective insulin resistance (IR) promote hepatic gluconeogenesis, glycolysis, and de novo lipogenesis; and excessive concentrations of free fatty acids from the diet and adipose tissue drive steatosis. Emerging evidence also implies that amino acid metabolism affects mitochondrial function and redox balance. Dysfunctional mitochondrial oxidative phosphorylation and the associated increase in reactive oxygen species production further exacerbate the cellular stress, inflammation, and fibrosis. However, compared with monosaccharide and fatty acid metabolism, the role of amino acid metabolism in MASLD/MASH remains less well understood. A better understanding of the role of such metabolic dysfunction in liver pathobiology should aid the identification of more useful biomarkers and precision therapies for MASLD/MASH.

Citations

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  • Precision medicine in steatotic liver disease
    Vitchapong Prasitsumrit, Vincent L. Chen
    Current Opinion in Gastroenterology.2026; 42(3): 121.     CrossRef
  • Immunometabolism of IRF4 in adipose, muscle, and immune cells influences obesity and MASLD
    Daniel M. Marko, Jonathan D. Schertzer
    American Journal of Physiology-Endocrinology and Metabolism.2026; 330(4): E520.     CrossRef
  • Colorimetric detection of amino acids enabled by functional nanomaterials: mechanisms, performance evaluation, and translational perspectives
    Wenfeng Ren, Wenyu Tu, Jiqiang Guo, Ying Gao
    Microchimica Acta.2026;[Epub]     CrossRef
  • 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
    Clinical and Molecular Hepatology.2026; 32(2): e136.     CrossRef
  • Metabolic features in plasma and urine of obese children and their association with MAFLD risk
    Shuang Hu, Wu Yan, Su Wu, Qianqi Liu, Xiaonan Li
    Frontiers in Nutrition.2026;[Epub]     CrossRef
  • Correspondence to letter to the editor on “Role of amino acids in the regulation of hepatic gluconeogenesis and lipogenesis in metabolic dysfunctionassociated steatotic liver disease”
    Eiji Kakazu, Masaaki Mino, Tatsuya Kanto
    Clinical and Molecular Hepatology.2026; 32(2): e235.     CrossRef
  • Blood Focused-Metabolomics and Transcriptomics Uncover Non-Linear Risk Association of Inadequate Dietary Choline Intake-Linked Metabolic Stress with MASLD Through Amino Acid Biomarkers, BCAA and MTORC 1/AKT1/IRS1 Mechanistic Mediators: A Nested Case–Contr
    Chien-Hsien Wu, Ming-Lu Lin, Chao-Yun Wang, Chi-Yang Chang, Fu-Jen Lee, Mei-Ling Cheng, Yu-Shun Lin, Tong-Wei Chen, Yi-Ting Hsiao, Bei-Wen Wang, Chang-Sheng Kuo, Rwei-Fen S. Huang
    International Journal of Molecular Sciences.2026; 27(10): 4186.     CrossRef
  • Methylcobalamin alleviates obesity through gut microbiota remodeling and modulation of bile acid-associated NF-κB signaling in mice
    Xuechun Zhang, Tong Wang, Han Li, Rongrong Ma, Xiaohua Pan, Chang Liu, Yaoqi Tian
    Food Bioscience.2026; 81: 109165.     CrossRef
  • Emerging insights into PPARα′s role in lean metabolic dysfunction-associated steatotic liver disease: Implications for targeted therapies
    Yafei Yang, Furong Zhang, Zhuang Peng, Yafei Wu, Ling Li, Zixia Shen, Qifa Ye, Jiang Yue, Shufang Na
    Acta Pharmaceutica Sinica B.2026;[Epub]     CrossRef
  • Targeting amino acid metabolism in hepatocellular carcinoma
    Yibing Wu, Carmen Chak-Lui Wong
    Trends in Molecular Medicine.2026;[Epub]     CrossRef
  • Unraveling the adverse outcome pathways of metabolic dysfunction-associated steatotic liver disease triggered by environmental mixtures via biological knowledge-driven machine learning
    Jiaming Fu, Guojie Qiao, Kerong Ma, Jinhao Jia, Honghui Li, Zeyang Bai, Limeng Xiong, Yuhan Zhang, Xiaozhe Geng, Hongju Duan, Yuxi Wang, Chunqing Gao, Xiaoyu Li, Yi Zhao, Hao Hu, Guangjun Wang, Rui Zhang, Yihong Di, Huifang Yang, Jian Sun
    Journal of Hazardous Materials.2026; 514: 142869.     CrossRef
  • Metainflammation, Mitochondrial Dysfunction, and Organokine Crosstalk: A Central Axis Linking Metabolic Syndrome to Cardiovascular Diseases
    Ana Flávia Pontes Sodré, Lucca Gonsales Rodrigues, Kátia P. Sloan, Lance A. Sloan, Masaru Tanaka, Rui Curi, Larissa Naomi Takeda, Ricardo de Alvares Goulart, Ana Luiza Decanini Miranda de Souza, Claudia Rucco Penteado Detregiachi, Antonelly Cassio Alves C
    International Journal of Molecular Sciences.2026; 27(15): 6554.     CrossRef
  • Dysregulation of Plasma Nonessential Amino Acids in Early‐Stage Type 2 Diabetes Mellitus
    Abdullah Abbas Hamzah Al-Rubaye, Walaa Esmail Jasim, Ahmed A. Mohsin, Nidhi Chaudhary
    Journal of Nutrition and Metabolism.2026;[Epub]     CrossRef
  • When the Liver Flares: Inflammatory and Immunometabolic Mechanisms Driving the Transition from MASLD to MASH
    Cristina Vecchio, Anteneh Nigussie Sheferaw, Emmanuel Kivumbi, Ian Stoppa, Deepika Pantham, Foteini Christaki, Alessia Provera, Umberto Dianzani, Salvatore Sutti
    Inflammation.2026;[Epub]     CrossRef
  • Food Nutrients and Bioactive Compounds for Managing Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comprehensive Review
    Erdenetsogt Dungubat, Kohei Fujikura, Masahiko Kuroda, Toshio Fukusato, Yoshihisa Takahashi
    Nutrients.2025; 17(13): 2211.     CrossRef
  • Current Data on the Role of Amino Acids in the Management of Obesity in Children and Adolescents
    Diana Zamosteanu, Nina Filip, Laura Mihaela Trandafir, Elena Ţarcă, Mihaela Pertea, Gabriela Bordeianu, Jana Bernic, Anne Marie Heredea, Elena Cojocaru
    International Journal of Molecular Sciences.2025; 26(15): 7129.     CrossRef
  • Protein and Macronutrient Metabolism in Liver Cirrhosis: About Sarcopenia
    Seul Ki Han, Soon Koo Baik, Moon Young Kim
    Nutrients.2025; 17(21): 3346.     CrossRef
  • 13,775 View
  • 333 Download
  • 20 Web of Science
  • Crossref

Original Article

Artificial intelligence, epidemiology, methodology, or others

Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta-oxidation
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
Clin Mol Hepatol 2025;31(2):445-459.
Published online December 23, 2024
DOI: https://doi.org/10.3350/cmh.2024.0642
Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a global epidemic. The disease 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 that promote this protection.
Methods
We downregulated MARC1 in primary human hepatocytes (PHHs) using short interfering RNA (siRNA). We measured neutral lipid content by Oil-Red O staining and fatty acid oxidation by radiolabeled tracers. We also performed RNA-sequencing and proteomic analysis using LC-MS. Additionally, we analyzed data from 239,075 participants from the UK Biobank.
Results
Downregulation of MARC1 reduced neutral lipid content in PHHs homozygous for the wild type (p.A165, risk), but not for the mutant (p.T165, protective), allele. We found that this reduction was mediated by increased fatty acid utilization via β-oxidation. Consistent with these results, we found that the levels of 3-hydroxybutyrate, a by-product of β-oxidation, were higher in carriers of the rs2642438 minor allele among samples from the UK biobank, indicating higher β-oxidation in these individuals. Moreover, downregulation of the 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, while upregulating beneficial pathways involved in cell survival.

Citations

Citations to this article as recorded by  Crossref logo
  • Loss of Mtarc1 Protects Against Steatotic Liver Disease in Mice
    Xiaofei Yin, Caroline Bickerton, Bryan MacDonald, Alessandro Arduini, Yunlong Shi, Mary Haas, Amy Deik, Mark Chaffin, Erika Kovacs‐Bogdan, Julian Avila Pacheco, Maiwen Amegadjie, Bidur Bhandary, Shayan Sadre, Thomas Rathjen, Irinna Papangeli, Raymond T. C
    Liver International.2026;[Epub]     CrossRef
  • MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease
    Meng Tie, Liwei Hu, Yunzhi Yang, Shaoxuan Song, Qihan Zhu, Jun Li, Wenjing Wang, Peng Xu, Juan Yu, Mengyue Wu, Tianheng Zhao, Delong Yuan, Hongyu Bao, Xiuyun Wang, Irfan J. Lodhi, Yong Chen, Yali Chen, Anyuan He
    Liver International.2026;[Epub]     CrossRef
  • Lactobacillus plantarum-fermented persimmon juice alleviates alcohol-induced hepatic ferroptosis by activating the Keap1/Nrf2 antioxidant axis
    Huijuan Kuang, Qingyuan Ye, Juan Tong, Hong Fu, Zhiqiang Shi, Bin Zhu, Guotai Yang
    Frontiers in Microbiology.2026;[Epub]     CrossRef
  • The many pathways driving liver inflammation in MASH
    Herbert Tilg, Timon E. Adolph, Stefano Romeo, Rohit Loomba
    Cell Metabolism.2026; 38(6): 1054.     CrossRef
  • Metabolic dysfunction-associated steatotic liver disease: On track to become the dominant etiology of hepatocellular carcinoma: Reply to correspondence on “Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta-
    Jian Xu, Wei Zhang, Guo Wu, Jingdong Li
    Clinical and Molecular Hepatology.2026; 32(2): e257.     CrossRef
  • Opportunities and challenges in controlling metabolic dysfunction-associated steatotic liver disease: Editorial on “Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta-oxidation”
    Jian Xu, Gang Shi, Tao Sheng, Jingdong Li
    Clinical and Molecular Hepatology.2026; 32(2): 919.     CrossRef
  • MTARC1 p.A165 ablation reduces hepatocellular carcinoma aggressiveness in vitro and in vivo
    Lohitesh Kovooru, Jingjing Zhang, Francesco Giuseppe Monni, Tanmoy Dutta, Xiangdong Gongye, Bernice Asiedu, Patrizia Infelise, Emelie Barreby, Oveis Jamialahmadi, Margit Mahlapuu, Rosellina M. Mancina, Stefano Romeo
    Clinical and Molecular Hepatology.2026; 32(2): 829.     CrossRef
  • Correspondence to editorial on “Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta-oxidation”
    Ester Ciociola, Tanmoy Dutta, Rosellina M. Mancina, Stefano Romeo
    Clinical and Molecular Hepatology.2026; 32(2): e216.     CrossRef
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    Julia Kozlitina, Stefano Romeo, Helen H. Hobbs
    Hepatology.2026;[Epub]     CrossRef
  • Mapping the genomic landscape of MASLD: A framework for molecular subtyping and precision hepatology
    Carlos José Pirola, Silvia Sookoian
    Med.2026; 7(6): 101131.     CrossRef
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    Nicholas O. Davidson
    Circulation Research.2026;[Epub]     CrossRef
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  • Correspondence to editorial 2 on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”
    Dongqin Yang, Yuli Lin, Chunhua Song, Ming Guan
    Clinical and Molecular Hepatology.2026; 32(3): e342.     CrossRef
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Editorial

Steatotic liver disease

Stabilizing hepatic fatty acid oxidation: Editorial on “USP29 alleviates the progression of MASLD by stabilizing ACSL5 through K48 deubiquitination”
Myeung Gi Choi, Na Young Lee, Ja Hyun Koo
Clin Mol Hepatol 2025;31(2):592-595.
Published online November 6, 2024
DOI: https://doi.org/10.3350/cmh.2024.0971

Citations

Citations to this article as recorded by  Crossref logo
  • JAB1/CRL4B complex represses PPARG/ACSL5 expression to promote breast tumorigenesis
    Ting Hu, Tianyu Ma, Miaomiao Huo, Jiaxiang Liu, Die Zhang, Yu Li, Jinyuan Chang, Min Zhang, Yinuo Wang, Tianyang Gao, Baowen Yuan, Siqi Wang, Qing Li, Xiaoqi Ma, Jingyao Zhang, Wei Huang, Yan Wang
    Cell Death & Differentiation.2026; 33(6): 1175.     CrossRef
  • Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction
    Wooyoung Choi, Gun Ha Woo, Tae-Hwan Kwon, Jae-Han Jeon
    International Journal of Molecular Sciences.2025; 26(19): 9715.     CrossRef
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  • 139 Download
  • 3 Web of Science
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Correspondence

Steatotic liver disease

PNPLA3 is one of the bridges between TM6SF2 E167K variant and MASLD: Correspondence to editorial on “TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD”
Baokai Sun, Likun Zhuang
Clin Mol Hepatol 2025;31(1):e67-e69.
Published online September 10, 2024
DOI: https://doi.org/10.3350/cmh.2024.0744
  • 6,130 View
  • 97 Download

Original Article

Steatotic liver disease

TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD
Baokai Sun, Xiaoqian Ding, Jie Tan, Jie Zhang, Xueru Chu, Shuimi Zhang, Shousheng Liu, Zhenzhen Zhao, Shiying Xuan, Yongning Xin, Likun Zhuang
Clin Mol Hepatol 2024;30(4):863-882.
Published online July 26, 2024
DOI: https://doi.org/10.3350/cmh.2024.0268
Backgrounds/Aims
Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant is closely associated with the occurrence and development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the role and mechanism of TM6SF2 E167K variant during MASLD progression are not yet fully understood.
Methods
The Tm6sf2167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC).
Results
The TM6SF2 E167K variant significantly aggravated hepatic steatosis and injury in HFD-induced mice. Decreased polyunsaturated PC level and increased polyunsaturated TG level were found in liver tissue of HFD-induced Tm6sf2167K KI mice. Mechanistic studies demonstrated that the TM6SF2 E167K variant increased the interaction between TM6SF2 and PNPLA3, and impaired PNPLA3-mediated transfer of polyunsaturated fatty acids (PUFAs) from TG to PC. The TM6SF2 E167K variant increased the level of fatty acid-induced malondialdehyde and reactive oxygen species, and decreased fatty acid-downregulated cell membrane fluidity. Additionally, the TM6SF2 E167K variant decreased the level of hepatic PC containing C18:3, and dietary supplementation of PC containing C18:3 significantly attenuated the TM6SF2 E167K-induced hepatic steatosis and injury in HFD-fed mice.
Conclusions
The TM6SF2 E167K variant could promote its interaction with PNPLA3 and inhibit PNPLA3-mediated transfer of PUFAs from TG to PC, resulting in the hepatic steatosis and injury during MASLD progression. PC containing C18:3 could act as a potential therapeutic supplement for MASLD patients carrying the TM6SF2 E167K variant.

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Snapshot

Steatotic liver disease

Immunopathogenesis of liver fibrosis in steatotic liver disease
Chaerin Woo, Won-Il Jeong
Clin Mol Hepatol 2024;30(2):299-302.
Published online February 19, 2024
DOI: https://doi.org/10.3350/cmh.2024.0113

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Reviews

Steatotic liver disease

NASH Therapy: omega 3 supplementation, vitamin E, insulin sensitizers and statin drugs
Stephen Caldwell
Clin Mol Hepatol 2017;23(2):103-108.
Published online May 10, 2017
DOI: https://doi.org/10.3350/cmh.2017.0103
Non-alcoholic steatohepatitis (NASH) is the more aggressive form of non-alcoholic fatty liver disease (NAFLD). NASH can progress to hepatic fibrosis, cirrhosis, portal hypertension and primary liver cancer. Therapy is evolving with a substantial number of trials of promising new agents now in progress. In this article however, we will examine data for several older forms of therapy which have been fairly extensively studied over the years: Polyunsaturated Fatty Acid (PUFA) supplements, vitamin E, insulin sensitizing agents with a focus on pioglitazone and statin agents. Early interest in PUFA derived from their potential benefit in cardio-metabolic disease and the close association of NAFLD/NASH with Metabolic Syndrome. Results have been variable although most studies show reduction of liver fat without other major effects and their effects are influenced by concomitant weight loss and underlying genetic factors. Vitamin E has had some efficacy in pediatric NASH but questionable efficacy in even mild NASH among adults. Pioglitazone has shown significant histological benefit in a number of trials but concern over side-effects (especially weight gain) have dampened enthusiasm. A newer insulin sensitizer, liraglutide, has also shown promise in a small randomized, controlled trial. Very limited data exists regarding the histological effects of the statins in NASH and these agents appear to be fairly neutral with neither clear cut benefit nor detriment. Their use is best guided by cardiovascular risks rather than liver histology.

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Steatotic liver disease

Nonalcoholic fatty liver disease: molecular mechanisms for the hepatic steatosis
Seung-Hoi Koo
Clin Mol Hepatol 2013;19(3):210-215.
Published online September 30, 2013
DOI: https://doi.org/10.3350/cmh.2013.19.3.210

Liver plays a central role in the biogenesis of major metabolites including glucose, fatty acids, and cholesterol. Increased incidence of obesity in the modern society promotes insulin resistance in the peripheral tissues in humans, and could cause severe metabolic disorders by inducing accumulation of lipid in the liver, resulting in the progression of non-alcoholic fatty liver disease (NAFLD). NAFLD, which is characterized by increased fat depots in the liver, could precede more severe diseases such as non-alcoholic steatohepatitis (NASH), cirrhosis, and in some cases hepatocellular carcinoma. Accumulation of lipid in the liver can be traced by increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, or the increased incidence of de novo lipogenesis. In this review, I would like to focus on the roles of individual pathways that contribute to the hepatic steatosis as a precursor for the NAFLD.

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    Eun-Young Park, Hojung Choi, Ji-Young Yoon, In-Young Lee, Youngwan Seo, Hong-Seop Moon, Jong-Hee Hwang, Hee-Sook Jun
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