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Editorial
. 2018 Nov;6(Suppl 1):S55.
doi: 10.21037/atm.2018.10.31.

Cholesterol homeostasis, macrophage malfunction and age-related macular degeneration

Mei Chen  1 , Chi-Chao Chan  2 , Heping Xu  1   3
Affiliations
Editorial

Cholesterol homeostasis, macrophage malfunction and age-related macular degeneration

Mei Chen et al. Ann Transl Med. 2018 Nov.
No abstract available

PubMed Disclaimer

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Cholesterol homeostasis and macrophage malfunction at the retina-choroidal interface in age-related macular degeneration. Photoreceptors acquire cholesterols and fatty acids from choroidal circulation or synthesize internally using acetyl-CoA to maintain the high-rate of photoreceptor outer segment (POS) turnover. The POS is phagocytized and digested by RPE cells. Retinal waste materials are dumped to choroid and then removed by choroidal macrophages. During aging, RPE function declines leading to the accumulation of undigested POS at the subretinal space or within RPE cells (in the form of lipofuscin). Macrophages and microglia migrate to subretinal space to remove undigested lipid-rich POS and damaged RPE debris. Macrophages may also migrate to sub-RPE space to remove debris. In AMD, macrophages are unable to maintain intracellular cholesterol/fatty acid homeostasis resulting in the accumulation of oxidized fatty acid (e.g., oxysterol). Intracellular oxysterol may activate various signalling pathways leading to macrophage malfunction. These include (I) reduced phagocytosis, which may be related to drusen formation; (II) uncontrolled inflammatory cytokine production, which may lead to RPE and photoreceptor death and the development of dry AMD; (III) the production of pro-angiogenic growth factors, which may induce wet AMD. ApoRPE, apoptotic RPE; BM, Bruch’s membrane; Cap, choriocapillaris; CNV, choroidal neovascularization; Dr, drusen; MФ, macrophages; RPE, retinal pigment epithelium.
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