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. Author manuscript; available in PMC: 2020 Oct 5.
Published in final edited form as: Curr Opin Lipidol. 2020 Apr;31(2):104–107. doi: 10.1097/MOL.0000000000000666

Fig. 1. NO2-FAs for the co-treatment of atherosclerosis and NAFLD: molecular and metabolic mechanisms.

Fig. 1.

ALT, alanine aminotransferase; AST, aspartate aminotransferase; COL1A, collagen, type I, alpha; CTGF, connective tissue growth factor; GCLC, glutamate-cysteine ligase catalytic subunit; GCLM, glutamate-cysteine ligase regulatory subunit; GPAT2, glycerol-3-phosphate acyltransferase-2; GSH, glutathione; GSR, glutathione reductase; HMOX1, heme oxygenase-1; ICAM1, intercellular adhesion molecule-1; IL-6, interleukin 6; MCP-1, monocyte chemoattractant protein-1; NAFLD, non-alcoholic fatty liver disease; NF-κB, nuclear factor kappa B; NQO1, NAD(P)H quinone dehydrogenase-1; Nrf2, nuclear factor erythroid 2-related factor-2; OxLDL, oxidized low-density lipoprotein; PON2, paraoxonase-2; ROS, reactive oxygen species; SCD-1, stearoyl-CoA desaturase-1; SREBF1, sterol regulatory element-binding transcription factor-1; SREBP1, sterol regulatory element-binding protein-1; STAT-1, signal transducer and activator of transcription-1; TGFB1, transforming growth factor beta-1; TIMP1, TIMP metallopeptidase inhibitor-1; TLR, toll-like receptor; Tumor necrosis factor; VCAM1, vascular cell adhesion molecule-1.