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Estrogen dysregulation, intraocular pressure, and glaucoma risk.
Youngblood, Hannah; Schoenlein, Patricia V; Pasquale, Louis R; Stamer, W Daniel; Liu, Yutao.
Afiliación
  • Youngblood H; Department of Cellular Biology and Anatomy, Augusta University, Augusta, GA, USA.
  • Schoenlein PV; Department of Cellular Biology and Anatomy, Augusta University, Augusta, GA, USA; Department of Radiology and Georgia Cancer Center, Augusta University, Augusta, GA, USA; Department of Surgery, Augusta University, Augusta, GA, USA.
  • Pasquale LR; Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
  • Stamer WD; Department of Ophthalmology and Biomedical Engineering, Duke University, Durham, NC, USA.
  • Liu Y; Department of Cellular Biology and Anatomy, Augusta University, Augusta, GA, USA; James and Jean Culver Vision Discovery Institute, Medical College of Georgia, Augusta University, Augusta, GA, USA; Center for Biotechnology and Genomic Medicine, Augusta University, Augusta, GA, USA. Electronic addres
Exp Eye Res ; 237: 109725, 2023 12.
Article en En | MEDLINE | ID: mdl-37956940
Characterized by optic nerve atrophy due to retinal ganglion cell (RGC) death, glaucoma is the leading cause of irreversible blindness worldwide. Of the major risk factors for glaucoma (age, ocular hypertension, and genetics), only elevated intraocular pressure (IOP) is modifiable, which is largely regulated by aqueous humor outflow through the trabecular meshwork. Glucocorticoids such as dexamethasone have long been known to elevate IOP and lead to glaucoma. However, several recent studies have reported that steroid hormone estrogen levels inversely correlate with glaucoma risk, and that variants in estrogen signaling genes have been associated with glaucoma. As a result, estrogen dysregulation may contribute to glaucoma pathogenesis, and estrogen signaling may protect against glaucoma. The mechanism for estrogen-related protection against glaucoma is not completely understood but likely involves both regulation of IOP homeostasis and neuroprotection of RGCs. Based upon its known activities, estrogen signaling may promote IOP homeostasis by affecting extracellular matrix turnover, focal adhesion assembly, actin stress fiber formation, mechanosensation, and nitric oxide production. In addition, estrogen receptors in the RGCs may mediate neuroprotective functions. As a result, the estrogen signaling pathway may offer a therapeutic target for both IOP control and neuroprotection. This review examines the evidence for a relationship between estrogen and IOP and explores the possible mechanisms by which estrogen maintains IOP homeostasis.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Glaucoma / Presión Intraocular Límite: Humans Idioma: En Revista: Exp Eye Res Año: 2023 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Glaucoma / Presión Intraocular Límite: Humans Idioma: En Revista: Exp Eye Res Año: 2023 Tipo del documento: Article País de afiliación: Estados Unidos