Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPAR<i>δ</i>-AMPK-PGC-1<i>α</i> Pathway in Dyslipidemic Conditions

<div>Hypothetical action mechanism of aspirin on nonalcoholic fatty liver and atherosclerosis. Simultaneous amelioration of both nonalcoholic fatty liver and atherosclerosis by aspirin is mainly achieved by catabolic activation, anti-inflammation, or vasodilation, which are the result of sequential regulation of the PPAR<i>δ</i>→p-AMPK→PGC-1<i>α</i>→oxidative phosphorylation pathway. In addition, the effects of aspirin are achieved by macrophage modulations, which include the increase of mannose receptor and decrease of CCR2.</div>

BioMed Research International

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Figure 9

Figure 9: Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPAR<i>δ</i>-AMPK-PGC-1<i>α</i> Pathway in Dyslipidemic Conditions 

Figure 9 | Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARδ-AMPK-PGC-1α Pathway in Dyslipidemic Conditions 