FIG. 4.

Possible therapeutic strategies involving lipids to prevent AMD development and progression. Based on previous AMD mouse model studies, we propose 3 therapeutic strategies involving lipids. Left: Targeting pathogenic lipid species in sub-RPE deposits by preventing their accumulation or removing them may reduce their ability to induce an inflammatory response in the sub-RPE milieu, to cause RPE damage, and may impede the development of AMD. Middle: Lipid homeostasis in the RPE is modulated by the actions of various transcription factors such as SREBPs, LXRs, and RXRs as well as autophagy. It is known that aging disrupts the signaling associated with these transcription factors and autophagic processes. Restoring these pathways may serve as valuable therapeutics in preventing AMD. Right: Mitochondria are important regulators of lipid oxidation. With age, mitochondria number and function decline in the RPE that may predispose the eye to AMD. By preserving or augmenting mitochondrial function, the RPE may remain healthy and avoid the dysfunction seen in AMD. LXRs, liver x receptors; RXRs, retinoid X receptors; SREBPs, sterol regulatory element-binding proteins.