SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in mice

IntroductionNonalcoholic steatohepatitis (NASH), characterized by progressive liver injury, inflammation, and fibrosis, is a leading chronic liver disease worldwide. Pharmacotherapy for NASH is thus urgently needed. Through a strategy of in vivo lineage tracing, it was recently discovered that delet...

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Main Authors: Lanzexin Yang, Shixuan Zhuo, Xinyu Zhu, Xinhui Zhang, Zinan Wang, Yan Chen
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-06-01
Series:Frontiers in Endocrinology
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Online Access:https://www.frontiersin.org/articles/10.3389/fendo.2025.1480453/full
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author Lanzexin Yang
Shixuan Zhuo
Xinyu Zhu
Xinhui Zhang
Zinan Wang
Yan Chen
Yan Chen
author_facet Lanzexin Yang
Shixuan Zhuo
Xinyu Zhu
Xinhui Zhang
Zinan Wang
Yan Chen
Yan Chen
author_sort Lanzexin Yang
collection DOAJ
description IntroductionNonalcoholic steatohepatitis (NASH), characterized by progressive liver injury, inflammation, and fibrosis, is a leading chronic liver disease worldwide. Pharmacotherapy for NASH is thus urgently needed. Through a strategy of in vivo lineage tracing, it was recently discovered that deletion of a protein methyltransferase SMYD2 has a protective role in hepatic steatosis. In this study, we evaluated the potential therapeutic effect of two SMYD2 inhibitors AZ505 and LLY-507 in a mouse NASH model.MethodsThe mouse NASH model was induced by a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 12 weeks. SMYD2 inhibitors AZ505 and LLY-507 were administered in the last 4 weeks at a dose of 10 mg/kg by intraperitoneal injection three times per week. A series of biochemical and histological analyses were conducted to determine the therapeutic potential of SMYD2 inhibitors.ResultsThe inhibitory effect of AZ505 and LLY-507 on histone methylation was confirmed with liver samples. CDAHFD was able to induce marked liver fibrosis and inflammation in the mice. However, treatment of the mice with AZ505 and LLY-507 failed to show any improvement in NASH scores, liver damage, liver fibrosis, macrophage infiltration, or hepatic inflammation in mice.DiscussionIn conclusion, our findings suggest that SMYD2 inhibition is not an effective strategy to alleviate NASH at least in mice.
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spelling doaj-art-5e91cea10fcd481da53403121b0f36972025-08-20T02:03:25ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922025-06-011610.3389/fendo.2025.14804531480453SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in miceLanzexin Yang0Shixuan Zhuo1Xinyu Zhu2Xinhui Zhang3Zinan Wang4Yan Chen5Yan Chen6Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, ChinaShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, ChinaSchool of Clinical Medicine, Gannan Medical University, Ganzhou, Jiangxi, ChinaShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, ChinaShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, ChinaShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, ChinaSchool of Clinical Medicine, Gannan Medical University, Ganzhou, Jiangxi, ChinaIntroductionNonalcoholic steatohepatitis (NASH), characterized by progressive liver injury, inflammation, and fibrosis, is a leading chronic liver disease worldwide. Pharmacotherapy for NASH is thus urgently needed. Through a strategy of in vivo lineage tracing, it was recently discovered that deletion of a protein methyltransferase SMYD2 has a protective role in hepatic steatosis. In this study, we evaluated the potential therapeutic effect of two SMYD2 inhibitors AZ505 and LLY-507 in a mouse NASH model.MethodsThe mouse NASH model was induced by a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 12 weeks. SMYD2 inhibitors AZ505 and LLY-507 were administered in the last 4 weeks at a dose of 10 mg/kg by intraperitoneal injection three times per week. A series of biochemical and histological analyses were conducted to determine the therapeutic potential of SMYD2 inhibitors.ResultsThe inhibitory effect of AZ505 and LLY-507 on histone methylation was confirmed with liver samples. CDAHFD was able to induce marked liver fibrosis and inflammation in the mice. However, treatment of the mice with AZ505 and LLY-507 failed to show any improvement in NASH scores, liver damage, liver fibrosis, macrophage infiltration, or hepatic inflammation in mice.DiscussionIn conclusion, our findings suggest that SMYD2 inhibition is not an effective strategy to alleviate NASH at least in mice.https://www.frontiersin.org/articles/10.3389/fendo.2025.1480453/fullSMYD2non-alcoholic steatohepatitisliver injuryfibrosisinflammationhepatic steatosis
spellingShingle Lanzexin Yang
Shixuan Zhuo
Xinyu Zhu
Xinhui Zhang
Zinan Wang
Yan Chen
Yan Chen
SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in mice
Frontiers in Endocrinology
SMYD2
non-alcoholic steatohepatitis
liver injury
fibrosis
inflammation
hepatic steatosis
title SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in mice
title_full SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in mice
title_fullStr SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in mice
title_full_unstemmed SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in mice
title_short SMYD2 inhibitors have no effect in improving non-alcoholic steatohepatitis in mice
title_sort smyd2 inhibitors have no effect in improving non alcoholic steatohepatitis in mice
topic SMYD2
non-alcoholic steatohepatitis
liver injury
fibrosis
inflammation
hepatic steatosis
url https://www.frontiersin.org/articles/10.3389/fendo.2025.1480453/full
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