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Mechanisms of Sodium-Driven Glial Dysfunction in Hypertensive Retinopathy

Award Number: R01EY039212
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/15/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2031

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Mechanisms of Sodium-Driven Glial Dysfunction in Hypertensive Retinopathy - Project Summary Hypertensive retinopathy is a prevalent yet often overlooked cause of vision loss, and vision loss disproportionately affects individuals with salt-sensitive hypertension. While research has primarily centered on vascular and angiogenic processes, new findings indicate that Müller glia, essential for regulating neurovascular coupling and ion balance in the retina, could be vital in connecting systemic sodium intake with retinal impairment. The epithelial sodium channel, a sodium-selective ion channel expressed in Müller glia, is upregulated in salt-sensitive but not salt-resistant hypertension and drives inflammation and tissue remodeling in other organs. Elevated intracellular sodium may also disrupt calcium signaling via reversal of the sodium/calcium exchanger, leading to glial calcium overload, altered synaptic support, and vascular instability. Given anatomical position and function, Müller glia may integrate systemic and local stressors to mediate retinal vascular and neuronal dysfunction. This project investigates how high salt intake alters glial sodium handling, promotes gliovascular uncoupling, and disrupts retinal function, specifically in salt-sensitive compared to salt-resistant phenotypes. This project will investigate how excess dietary salt contributes to vision loss by disrupting the function of Müller glial cells, key regulators of the retina’s vascular and neuronal health. The central hypothesis is that salt-sensitive stress impairs glial signaling, weakening the protective barrier in the retina and interfering with normal visual processing. Aim 1 will examine how salt affects sodium regulation in glial cells. Aim 2 will test whether glial reactivity contributes to breakdown of the blood-retina barrier. Aim 3 will explore how salt-induced changes in glial activity affect visual function. Together, these studies will define new mechanisms of retinal injury relevant to hypertension and may identify novel glial-targeted strategies to prevent vision loss in at-risk populations. My Stephen I. Katz Early-Stage Investigator R01 project represents a new scientific direction and substantive shift from my prior research, which focused on innate immune-mediated mechanisms of hypertension and the NLRP3 (NODD- LRR- pyrin domain-containing 3) in myeloid cells. By shifting to neuroglial regulation of retinal injury, this project expands my scientific trajectory into the retina and neurovascular biology, fulfilling the intent of the Katz R01 mechanism to support early-stage investigators pursuing innovative, independent research. The proposed studies will establish a new glial-centric framework for hypertensive retinopathy, uncover strain- and sodium-dependent mechanisms of retinal injury, and identify novel therapeutic targets to prevent vision loss in salt-sensitive individuals.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $654,161 )
2026	2026	MEHARRY MEDICAL COLLEGE	1005 DR DB TODD JR BLVD	NASHVILLE	TN	37208	DAVIDSON	USA	Vision Research	000	1	9/10/2026	NEW	$654,161
														Subtotal = $654,161

Grand Total All Awards = $654,161

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Mechanisms of Sodium-Driven Glial Dysfunction in Hypertensive Retinopathy

Award Number: R01EY039212

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/15/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2031

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