Cargando…

Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited

Diabetic retinopathy (DR) and diabetic macular edema (DME) are major causes for visual loss in adults. Nearly half of the world’s population with diabetes has some degree of DR, and DME is a major cause of visual impairment in these patients. Severe vision loss occurs because of tractional retinal d...

Descripción completa

Detalles Bibliográficos
Autores principales: Triebel, Jakob, Bertsch, Thomas, Clapp, Carmen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9500238/
https://www.ncbi.nlm.nih.gov/pubmed/36157442
http://dx.doi.org/10.3389/fendo.2022.994898
_version_ 1784795173450940416
author Triebel, Jakob
Bertsch, Thomas
Clapp, Carmen
author_facet Triebel, Jakob
Bertsch, Thomas
Clapp, Carmen
author_sort Triebel, Jakob
collection PubMed
description Diabetic retinopathy (DR) and diabetic macular edema (DME) are major causes for visual loss in adults. Nearly half of the world’s population with diabetes has some degree of DR, and DME is a major cause of visual impairment in these patients. Severe vision loss occurs because of tractional retinal detachment due to retinal neovascularization, but the most common cause of moderate vision loss occurs in DME where excessive vascular permeability leads to the exudation and accumulation of extracellular fluid and proteins in the macula. Metabolic control stands as an effective mean for controlling retinal vascular alterations in some but not all patients with diabetes, and the search of other modifiable factors affecting the risk for diabetic microvascular complications is warranted. Prolactin (PRL) and its proteolytic fragment, vasoinhibin, have emerged as endogenous regulators of retinal blood vessels. PRL acquires antiangiogenic and anti-vasopermeability properties after undergoing proteolytic cleavage to vasoinhibin, which helps restrict the vascularization of ocular organs and, upon disruption, promotes retinal vascular alterations characteristic of DR and DME. Evidence is linking PRL (and other pituitary hormones) and vasoinhibin to DR and recent preclinical and clinical evidence supports their translation into novel therapeutic approaches.
format Online
Article
Text
id pubmed-9500238
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-95002382022-09-24 Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited Triebel, Jakob Bertsch, Thomas Clapp, Carmen Front Endocrinol (Lausanne) Endocrinology Diabetic retinopathy (DR) and diabetic macular edema (DME) are major causes for visual loss in adults. Nearly half of the world’s population with diabetes has some degree of DR, and DME is a major cause of visual impairment in these patients. Severe vision loss occurs because of tractional retinal detachment due to retinal neovascularization, but the most common cause of moderate vision loss occurs in DME where excessive vascular permeability leads to the exudation and accumulation of extracellular fluid and proteins in the macula. Metabolic control stands as an effective mean for controlling retinal vascular alterations in some but not all patients with diabetes, and the search of other modifiable factors affecting the risk for diabetic microvascular complications is warranted. Prolactin (PRL) and its proteolytic fragment, vasoinhibin, have emerged as endogenous regulators of retinal blood vessels. PRL acquires antiangiogenic and anti-vasopermeability properties after undergoing proteolytic cleavage to vasoinhibin, which helps restrict the vascularization of ocular organs and, upon disruption, promotes retinal vascular alterations characteristic of DR and DME. Evidence is linking PRL (and other pituitary hormones) and vasoinhibin to DR and recent preclinical and clinical evidence supports their translation into novel therapeutic approaches. Frontiers Media S.A. 2022-09-09 /pmc/articles/PMC9500238/ /pubmed/36157442 http://dx.doi.org/10.3389/fendo.2022.994898 Text en Copyright © 2022 Triebel, Bertsch and Clapp https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Triebel, Jakob
Bertsch, Thomas
Clapp, Carmen
Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited
title Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited
title_full Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited
title_fullStr Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited
title_full_unstemmed Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited
title_short Prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited
title_sort prolactin and vasoinhibin are endogenous players in diabetic retinopathy revisited
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9500238/
https://www.ncbi.nlm.nih.gov/pubmed/36157442
http://dx.doi.org/10.3389/fendo.2022.994898
work_keys_str_mv AT triebeljakob prolactinandvasoinhibinareendogenousplayersindiabeticretinopathyrevisited
AT bertschthomas prolactinandvasoinhibinareendogenousplayersindiabeticretinopathyrevisited
AT clappcarmen prolactinandvasoinhibinareendogenousplayersindiabeticretinopathyrevisited