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©The Author(s) 2022.
World J Gastroenterol. Jul 7, 2022; 28(25): 2937-2954
Published online Jul 7, 2022. doi: 10.3748/wjg.v28.i25.2937
Published online Jul 7, 2022. doi: 10.3748/wjg.v28.i25.2937
Figure 5 The activity of fatty acid synthesis was enhanced in TM6SF2 knockdown group.
A: Pathway enrichment of the up-regulated differentially expressed genes by Kyoto Encyclopedia of Genes and Genomes analysis; B: Microarray heatmap of genes involved in fatty acid metabolism in TM6SF2-knockdown cells; C: The SREBP-1c target protein levels in L02 and HepG2 cells after palmitic acid (PA) treatment; D: The SREBP-1c target protein levels in TM6SF2-knockdown cells after PA treatment; E: Immunoblot analysis of SREBP-1c in cytoplasmic and nuclear extracts; F: Hepatic malonyl-CoA contents of mice in two groups (n = 5 mice per group); G: The mRNA levels of genes involved in fatty acid synthesis (Srebf1, Fasn, Scd1, Acaca and Hmgcr) and uptake (Cd36, Slc27a1 and Fabp1). aP < 0.05; bP < 0.01; cP < 0.001. HFD: High-fat diet; PA: Palmitic acid; ACC: Acetyl-CoA carboxylase; μM: μmol/L.
- Citation: Li ZY, Wu G, Qiu C, Zhou ZJ, Wang YP, Song GH, Xiao C, Zhang X, Deng GL, Wang RT, Yang YL, Wang XL. Mechanism and therapeutic strategy of hepatic TM6SF2-deficient non-alcoholic fatty liver diseases via in vivo and in vitro experiments. World J Gastroenterol 2022; 28(25): 2937-2954
- URL: https://www.wjgnet.com/1007-9327/full/v28/i25/2937.htm
- DOI: https://dx.doi.org/10.3748/wjg.v28.i25.2937