ArticleCellular and molecular life sciences : CMLS2025
Linc01271 promotes lipid synthesis and MASLD/MASH progression via miR-149-3p/RAB35 axis.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic associated steatohepatitis (MASH) is a severe form of metabolic dysfunction-associated steatotic liver disease (MASLD) characterized by hepatocellular injury, inflammation, and fibrosis. Despite advances in understanding its pathophysiology, the molecular mechanisms driving MASH progression remain unclear. This study investigates the role of long non-coding RNA Linc01271 in MASLD/MASH pathogenesis, ant its involvement in the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR signaling pathway. Transcriptome sequencing and RT-qPCR revealed significant upregulation of Linc01271 in MASH tissues, which correlated with lipid accumulation and inflammatory responses. Knockdown of Linc01271 in THLE-2 cells reduced lipid droplet formation, triglyceride and cholesterol levels, and the expression of lipid metabolism-related genes (CD36, ACC1, FASN) and pro-inflammatory cytokines (IL-6, IL-8, TGF-β1). Conversely, Linc01271 overexpression had the opposite effect. Dual-luciferase reporter assays confirmed Linc01271's interaction with miR-149-3p, which regulates RAB35, a downstream target of miR-149-3p. Knockdown of Linc01271 in mice attenuated MASH progression, reducing body weight, liver weight, blood glucose levels, and liver injury markers. These findings demonstrate that Linc01271 promotes lipid synthesis and inflammatory responses through the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR pathway, highlighting its potential as a therapeutic target for MASLD/MASH. Further research is warranted to develop therapeutic agents targeting Linc01271 for clinical applications.
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