Figure 1. The role of OxPLs in pathogenesis of AMD and the main functions of MET to prevent and treat AMD.

Lipid accumulation resulted from aging of RPE on one hand leads to the thickening of Bruch's membrane, which further leads to choroidal hypoxia, the expression of HIF-1 and VEGF, and ultimately the formation of CNV; on the other hand, it leads to the formation of drusen, which is the hallmark of early AMD. OxPLs in drusen induce inflammation and oxidative stress, which further cause programmed cell death, such as pyroptosis and apoptosis of RPE cells. Pyroptotic cell in turn aggravates inflammation by releasing pro-inflammation factors, and further promotes CNV formation. The death of RPE cells leads to the degeneration of the neuroretina. CNV formation and retinal degeneration mark the late stage of AMD. MET can activate AMPK. AMPK activation can reduce lipid accumulation through AMPK/LXR pathway, suppress inflammation, prohibit retinal cells from death, and inhibit CNV formation, thus to prevent and treat AMD. OxPLs: Oxidized phospholipids; RPE: Retinal pigment epithelium; AMPK: Adenosine monophosphate-activated protein kinase; LXR: Liver X receptor; HIF-1: Hypoxia inducible factor-1; VEGF: Vascular endothelial growth factor; AMD: Age-related macular degeneration; CNV: Choroidal neovascularization.