The Retinal Renin-Angiotensin-Aldosterone System: Implications for Glaucoma.
glaucoma
oxidative stress
primary aldosteronism
renin-angiotensin-aldosterone system
Journal
Antioxidants (Basel, Switzerland)
ISSN: 2076-3921
Titre abrégé: Antioxidants (Basel)
Pays: Switzerland
ID NLM: 101668981
Informations de publication
Date de publication:
22 Mar 2022
22 Mar 2022
Historique:
received:
28
01
2022
revised:
18
03
2022
accepted:
18
03
2022
entrez:
23
4
2022
pubmed:
24
4
2022
medline:
24
4
2022
Statut:
epublish
Résumé
Aldosterone is one of the main effectors of the renin-angiotensin-aldosterone system (RAAS) along with having roles in hypertension, and cardiovascular and renal diseases. Recent evidence has also shown the presence of an active local RAAS within the human eye. It has been shown that at 12 h after a retinal ischemia-reperfusion injury, there is an upregulation of the protein levels of angiotensin II type 1 receptor (AT1-R) in the retina. Furthermore, at 12 h after reperfusion, there is an increase in reactive oxygen species (ROS) production in the retina that is mediated via an NADPH oxidase pathway. This ischemia-reperfusion injury-induced increase of retinal ROS levels and NADPH oxidase expression can be prevented by the administration of an AT1-R antagonist. This suggests that one of the main retinal ischemic injury pathways is via the local RAAS. It has also been reported that progressive retinal ganglion cell loss and glaucomatous optic nerve degeneration without elevated intraocular pressure occur after administration of local or systemic aldosterone. Elucidation of glaucoma pathogenesis, especially normal-tension glaucoma (NTG) subtype by our current animal model can be used for identifying potential therapeutic targets. Based on these results, we are further evaluating NTG prevalence among primary aldosteronism patients.
Identifiants
pubmed: 35453295
pii: antiox11040610
doi: 10.3390/antiox11040610
pmc: PMC9029628
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan
ID : 20K09827
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