Key result
Local retinal RAAS activation and aldosterone are linked to progressive normal-tension glaucoma.
Why the study?
Recent evidence demonstrates an active local RAAS in the human eye, prompting elucidation of glaucoma pathogenesis, particularly normal-tension glaucoma, to identify potential therapeutic targets.
This review highlights the potential role of the local retinal renin-angiotensin-aldosterone system, specifically aldosterone, in the pathogenesis of normal-tension glaucoma, suggesting a novel therapeutic target.
Supports retinal aldosterone as a novel target in normal-tension glaucoma; leaves open whether blockade slows ganglion cell loss.
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.
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Hirooka et al. (2022) conducted a review in Glaucoma. Aldosterone was evaluated. Aldosterone and the local retinal renin-angiotensin-aldosterone system are implicated in progressive retinal ganglion cell loss and the pathogenesis of normal-tension glaucoma independent of intraocular pressure.
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