From: Phosphorylation: new star of pathogenesis and treatment in steatotic liver disease
Category | Name | Treatment effect | Phosphorylation action site | Potential mechanism |
---|---|---|---|---|
Prescription | Metformin (+ genistein) [66] | Decreasing body and liver weight/fasting blood glucose/liver triglyceride level | p-GSK-3β/p-AMPK/p-NF-kB | Switching macrophage into M2 phenotype, decreasing macrophage infiltration, reducing pro-inflammatory cytokines via p-GSK3/p-AMPK/p-NF-kB |
Metformin (+ chlorogenic acid) [67] | Decreasing fasting blood glucose /hepatic triglyceride level/improving glucose intolerance | p-GSK-3β/p-AMPK | Resulting in the polarization of macrophages to the M2 phenotype, reducing pro-inflammatory cytokines and decreasing protein level of NF-kB via p-AMPK | |
Empagliflozin [84] | Potential treatments against NAFLD | p-AMPK | Decreasing the expression of ER transactivating autophagy via increasing p-AMPK, and reducing apoptosis | |
Dapagliflozin [27] | Anti-NAFLD/decreasing lipogenic enzyme | p-ACC1/p-mTOR/p-AMPK | Reducing hepatic lipid accumulation via promoting p-ACC1 and inducing autophagy via the AMPK-mTOR pathway | |
Silybin [40] | Anti-NAFLD efficacy by antioxidant/anti-inflammatory | p-JNK | Decreasing hepatic injury, lipid metabolism and oxidative stress by CFLAR-JNK pathway | |
Ursodeoxycholic Acid [86] | Anti-NAFLD efficacy by antioxidant/anti-inflammatory/preventing mitochondrial dysfunction | p-NF-kB/p-STAT3 | Increasing hepatic energy expenditure, mitochondria biogenesis, and incorporation of bile acid metabolism by downregulating p-NF-kB and p-STAT3 | |
Aspirin [87] | Normalize NAFLD and atherosclerosis | p-AMPK | Inhibiting lipid biosynthesis and inflammation and elevating catabolic metabolism via activation of the PPARδ-AMPK-PGC-1α pathway | |
Fenticonazole nitrate [88] | Anti-diabetic and anti-NAFLD efficacies | AKT Ser473/PPARγ Ser273 | Activating Adiponectin and GLUT4 by promoting the AKT at Ser473 site and blocking the PPARγ at Ser273 site via phosphorylation |