fig2

The roles of autophagy and thyroid hormone in the pathogenesis and treatment of NAFLD

Figure 2. TH effects on hepatic autophagy. TH increases transcription of genes involved in autophagy, mitochondrial biogenesis, and lipid metabolism. Increases in mitochondrial β-oxidation of fatty acids increase ROS which then serve as signaling molecules to activate the CAMKK2-AMPK-ULK1 pathway to stimulate lipophagy. Lipophagy mobilizes lipolysis of triglycerides stored in LDs as free fatty acids that act as fuel for mitochondrial utilization. ROS also activates mitophagy to remove damaged mitochondria. TH: Thyroid hormone; ROS: reactive oxygen species; LDs: lipid droplets; CAMKK2: calcium/calmodulin dependent protein kinase kinase 2; AMPK: AMP-activated protein kinase; ULK1: unc-51 like autophagy activating kinase 1.

Hepatoma Research
ISSN 2454-2520 (Online) 2394-5079 (Print)

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