ArticleAmerican journal of translational research2026
MCT4 alleviates lipid accumulation, inflammation and PANoptosis in non-alcoholic fatty liver disease by inhibiting JAK-STAT signaling transduction.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Targeting the non-coding RNA-PANoptosis axis: a novel frontier in disease diagnosis and therapy.Apoptosis : an international journal on programmed cell death · 2026Review
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10 authors.
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Abstract
objectivesTo investigate the role of monocarboxylate transporter 4 (MCT4) in non-alcoholic fatty liver disease (NAFLD) and its underlying mechanisms.
methodsPalmitic acid (PA) was used to stimulate L-02 cells, establishing an
resultsAfter PA treatment, the levels of triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) in cells increased, while the level of high-density lipoprotein cholesterol (HDL-C) decreased. The expression of lipid synthesis-related genes was upregulated, while the expression of lipid breakdown-related genes was downregulated. Similarly, PA induced cellular inflammatory infiltration and PANoptosis. However, overexpression of MCT4 reversed PA induced lipid accumulation and inflammatory response. Mechanistic studies demonstrated that MCT4 alleviated PA-induced lipid accumulation and inflammatory response by reducing the phosphorylation levels of JAK1 and STAT3. Compared with the model group, mice overexpressing MCT4 showed reduced liver tissue damage.
conclusionsMCT4 provides new reference for the treatment of NAFLD by inhibiting the JAK-STAT pathway, slowing down lipid accumulation and inflammatory response in NAFLD.
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