Epigenetics and Signaling Pathways in Glaucoma

Joint Authors

Liu, Ji
Gauthier, Angela C.

Source

BioMed Research International

Issue

Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-12, 12 p.

Publisher

Hindawi Publishing Corporation

Publication Date

2017-01-22

Country of Publication

Egypt

No. of Pages

12

Main Subjects

Medicine

Abstract EN

Glaucoma is the most common cause of irreversible blindness worldwide.

This neurodegenerative disease becomes more prevalent with aging, but predisposing genetic and environmental factors also contribute to increased risk.

Emerging evidence now suggests that epigenetics may also be involved, which provides potential new therapeutic targets.

These three factors work through several pathways, including TGF-β, MAP kinase, Rho kinase, BDNF, JNK, PI-3/Akt, PTEN, Bcl-2, Caspase, and Calcium-Calpain signaling.

Together, these pathways result in the upregulation of proapoptotic gene expression, the downregulation of neuroprotective and prosurvival factors, and the generation of fibrosis at the trabecular meshwork, which may block aqueous humor drainage.

Novel therapeutic agents targeting these pathway members have shown preliminary success in animal models and even human trials, demonstrating that they may eventually be used to preserve retinal neurons and vision.

American Psychological Association (APA)

Gauthier, Angela C.& Liu, Ji. 2017. Epigenetics and Signaling Pathways in Glaucoma. BioMed Research International،Vol. 2017, no. 2017, pp.1-12.
https://search.emarefa.net/detail/BIM-1137718

Modern Language Association (MLA)

Gauthier, Angela C.& Liu, Ji. Epigenetics and Signaling Pathways in Glaucoma. BioMed Research International No. 2017 (2017), pp.1-12.
https://search.emarefa.net/detail/BIM-1137718

American Medical Association (AMA)

Gauthier, Angela C.& Liu, Ji. Epigenetics and Signaling Pathways in Glaucoma. BioMed Research International. 2017. Vol. 2017, no. 2017, pp.1-12.
https://search.emarefa.net/detail/BIM-1137718

Data Type

Journal Articles

Language

English

Notes

Includes bibliographical references

Record ID

BIM-1137718