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. 2024 Apr 19;29(8):1859. doi: 10.3390/molecules29081859

Figure 2.

Figure 2

Potential mechanisms by which statins may favorably affect liver histology in NASH/NAFLD. This cartoon emphasizes the pleiotropic effects of statins on the liver and the potential mechanisms that may combine to ameliorate the primary pathological conditions of NASH/NAFLD, such as steatosis, inflammation, and fibrosis. The downward pointing arrow signifies downregulation. ACO, acyl-CoA oxidase; PON1, paraoxonase 1; PPAR, peroxisome proliferator-activated receptor; CPT, carnitine palmitoyltransferase; LKB1/AMPK, AMP-activated protein kinase; ALE-RAGE, advanced lipoxidation end product-receptors of advanced glycation end products; TNF, tumor necrosis factor; NLRP3, NOD-like receptor family pyrin domain-containing 3; IL-1β, cytokines interleukin (IL)-1β; GTPases, small guanine triphosphate-binding proteins; eNOS, endothelial nitric oxide synthase; iNOS, inducible nitric oxide synthase; LSECs, liver sinusoidal endothelial cells; KCs, Kupffer cells; HSCs, hepatic stellate cells; RAS/ERK; Ras-extracellular signal-regulated kinase.