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. 2023 May 2;10:1116861. doi: 10.3389/fcvm.2023.1116861

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© 2023 Finney, Das, Kumar, Mckinney, Cai, Yurdagul and Rom.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Biomarkers linking NAFLD/NASH and ASCVD offer potential therapeutic strategies. Lipid species that are increased in both NAFLD/NASH and ASCVD include low-density lipoprotein-cholesterol (LDL-C), very low-density lipoprotein (VLDL) and triglycerides (TG) as well as ceramides. Although significantly lowering ASCVD, LDL-C reduction using statins has shown inconsistent results with regards to NASH treatment. Targeting ceramide synthesis have shown promising results in rodent models of NAFLD/NASH and ASCVD and warrants clinical evaluation. Amino acid metabolism is commonly dysregulated in NAFLD/NASH and ASCVD with circulating branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs) increased and glycine decreased in both diseases. In rodent models and small-scale clinical studies, glycine-based treatments reduced steatohepatitis and atherosclerosis warranting clinical evaluation in larger cohorts. The hepatokines, fibroblast growth factor-21 (FGF-21) and angiopoietin like 3 (ANGPTL3), are increased in both NAFLD/NASH and ASCVD. Interestingly, approaches to inhibit hepatic ANGPTL3 have shown promise in treating dyslipidemia but were associated with increased hepatic steatosis and markers of liver injury. Despite being increased in both diseases, FGF21 analogues are protective in rodent models of NASH and atherosclerosis as well as in patients with NASH.