Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 May 11;8(2):31.
doi: 10.3390/biology8020031.

Mitochondrial Dysfunction in the Aging Retina

Affiliations
Review

Mitochondrial Dysfunction in the Aging Retina

Janis T Eells. Biology (Basel). .

Abstract

Mitochondria are central in retinal cell function and survival and they perform functions that are critical to cell function. Retinal neurons have high energy requirements, since large amounts of ATP are needed to generate membrane potentials and power membrane pumps. Mitochondria over the course of aging undergo a number of changes. Aged mitochondria exhibit decreased rates of oxidative phosphorylation, increased reactive oxygen species (ROS) generation and increased numbers of mtDNA mutations. Mitochondria in the neural retina and the retinal pigment epithelium are particularly susceptible to oxidative damage with aging. Many age-related retinal diseases, including glaucoma and age-related macular degeneration, have been associated with mitochondrial dysfunction. Therefore, mitochondria are a promising therapeutic target for the treatment of retinal disease.

Keywords: age-related macular degeneration; aging; diabetic retinopathy; glaucoma; mitochondria; optic nerve; retina.

PubMed Disclaimer

Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
Anatomy of the retina and the structure of rod and cone photoreceptors.
Figure 2
Figure 2
Mitochondria in the aging retina. Mitochondria are essential for many cellular functions including: (1) the synthesis of ATP by oxidative phosphorylation, (2) the regulation of intracellular calcium homeostasis, (3) anterograde and retrograde signaling between the nucleus and mitochondria, (4) the generation of reactive oxygen species (ROS) from the electron transport chain (ETC). ROS act as signaling molecules in low concentrations or as toxic molecules in higher concentrations. ROS oxidize mitochondrial lipids, proteins and DNA and (5) the regulation of apoptosis. Excess ROS or intramitochondrial calcium can lead to the activation of cell death pathways by opening the mitochondrial permeability transition pore (PTP).
Figure 3
Figure 3
Mitochondrial involvement in dry age-related macular degeneration (AMD).
Figure 4
Figure 4
Mitochondrial dysfunction in glaucoma.

References

    1. Sung C.H., Chuang J.Z. The cell biology of vision. J. Cell Biol. 2010;190:953–963. doi: 10.1083/jcb.201006020. - DOI - PMC - PubMed
    1. Winkler B.S. Glycolytic and oxidative metabolism in relation to retinal function. J. Gen. Physiol. 1981;77:667–692. doi: 10.1085/jgp.77.6.667. - DOI - PMC - PubMed
    1. Warbug O. Uber die klassifizierung tierischer gewebe nach ihrem stoffwechsel. Biochem. Z. 1927;184:484–488.
    1. Ames A., 3rd, Li Y.Y., Heher E.C., Kimble C.R. Energy metabolism of rabbit retina as related to function: High cost of sodium transport. J. Neurosci. 1992;12:840–853. doi: 10.1523/JNEUROSCI.12-03-00840.1992. - DOI - PMC - PubMed
    1. Medrano C.J., Fox D.A. Oxygen consumption in the rat outer and inner retina: Light- and pharmacologically-induced inhibition. Exp. Eye Res. 1995;61:273–284. doi: 10.1016/S0014-4835(05)80122-8. - DOI - PubMed

LinkOut - more resources