Evidence map›Paper›PMID 42499162›Full record

ArticleClinical and translational medicine2026

Role of LncSNHG5 in MAFLD: Mechanisms of Arid1a K391 lactylation and lipid accumulation.

Xinmiao Li, Feng Jiang, Binbo Fang, Lifan Lin, Jianjian Zheng, Tanzhou Chen

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Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Xinmiao LiDepartment of Clinical Laboratory, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Feng JiangZhejiang Key Laboratory of Intelligent Cancer Biomarker Discovery and Translation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Binbo FangZhejiang Key Laboratory of Intelligent Cancer Biomarker Discovery and Translation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0003-1311-6769
Lifan LinDepartment of Clinical Laboratory, The Third Affiliated Hospital of Wenzhou Medical University, Ruian, China.
Jianjian ZhengZhejiang Key Laboratory of Intelligent Cancer Biomarker Discovery and Translation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Tanzhou ChenDepartment of Gastroenterology and Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0002-8307-2389

Funding

Joint Project of the Zhejiang Provincial Natural Science Foundation LBY24H200005Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province 2022E10022Major Projects of Wenzhou Science and Technology Bureau ZY2024005National Natural Science Foundation of China 81873576Zhejiang Provincial Medical and Health Planning Project 2025KY102
6 · The paper itself

Abstract

introductionMetabolic dysfunction-associated fatty liver disease (MAFLD) is a common chronic liver condition marked by abnormal lipid metabolism.

objectivesSmall nucleolar RNA host gene 5 (SNHG5) is involved in the regulation of cell proliferation and apoptosis and was previously identified as a profibrotic factor in liver fibrosis. However, its role in MAFLD remains unclear. This study aimed to elucidate the contribution of SNHG5 to MAFLD progression. METHODS AND

resultsSNHG5 expression was markedly elevated during MAFLD progression, whereas SNHG5 inhibition suppressed lipid accumulation. Transcriptomic sequencing of primary hepatocytes overexpressing SNHG5 demonstrated significant downregulation of monocarboxylate transporter 1 (MCT1), a key lactate transporter. Integrated lactyl-proteomic and proteomic analyses further revealed that SNHG5 overexpression promoted lactylation of the non-histone protein AT-rich interaction domain 1A (Arid1a) at K391, thereby driving excessive lipid accumulation. Acyltransferase assays indicated that both P300 and HBO1 participated in SNHG5-mediated Arid1a lactylation. In vivo, hepatocyte-specific SNHG5 knockout markedly attenuated hepatic lipid accumulation and MAFLD progression, whereas simultaneous hepatocyte-specific deletion of SNHG5 and MCT1 restored lipid accumulation compared with SNHG5-deficient mice.

conclusionSNHG5 promotes lipid accumulation and MAFLD progression through induction of MCT1-mediated Arid1a K391 lactylation.

Indexed as

DNA-Binding ProteinsFatty LiverLipid MetabolismRNA, Small NucleolarTranscription FactorsAnimalsHepatocytesHumansMaleMiceDNA-Binding ProteinsRNA, Small NucleolarTranscription FactorsHBO1lactylationLncSNHG5MAFLDP300

Identifiers

PMID42499162
PMCPMC13400984

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