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Hormonal Dynamics and Extracellular Vesicle Function in Keratoconus: Exploring Pathophysiology and Developing Targeted Therapies

Award Number: K99EY037781
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2028

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Hormonal Dynamics and Extracellular Vesicle Function in Keratoconus: Exploring Pathophysiology and Developing Targeted Therapies - Summary: Keratoconus (KC) is a progressive corneal ectasia characterized by the degradation of stromal collagen. The pathophysiology of KC is intricate, involving a range of biochemical, immunological, metabolic, endocrinological, and genetic factors. Because of this complexity, the exact origin of the disease—whether it arises from the epithelium or the stroma—remains debated due to the lack of an appropriate disease model. KC generally begins after puberty, and can be exacerbated by pregnancy, and rarely progresses after menopause. Furthermore, there is a critical absence of reliable prognostic markers that could clarify why some KC patients experience faster progression than others. Our study will assess the impact of hormones such as follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, and progesterone—individually or in combination—on collagen degradation. To address these challenges, we will utilize tears from both KC and non- KC patients (male and female), along with our developed 3D collagen hydrogel model of corneal epithelium and keratocytes. We will focus on the spatiotemporal regulation of matrix metalloproteinases (MMP-2/9) to identify the specific signaling pathways involved This endeavor could lead to developing topical therapeutic agents to mitigate hormone-mediated corneal thinning. Previous research has used KC tears to identify potential biomarkers for the disease, and extracellular vesicles (EVs) have been suggested as possible disease indicators. Male KC patients secrete increased EVs compared to their female counterparts. However, the functional roles of tear-derived EVs and their molecular constituents (RNA and protein) have yet to be explored. In this study, we will utilize tears KC and non-KC patients, along with our developed 3D collagen hydrogel model, to investigate how specific KC-associated mutations (lysyl oxidase rs2956540 and MMP9-rs17576) influence the differential sorting of miRNA in EVs. We will also examine the role of miRNA derived EVs from the tears of KC patients in the pathogenesis of corneal ectasia. Overall, the use of our 3D corneal model will allow us to identify cell-specific responses to hormones and EVs, providing insights into the origins of the disease pathology.


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 = $132,837 )
2026	2026	SCHEPENS EYE RESEARCH INSTITUTE, INC., THE	20 STANIFORD ST	BOSTON	MA	02114	SUFFOLK	USA	Vision Research	000	1	6/12/2026	NEW	$132,837
														Subtotal = $132,837

Grand Total All Awards = $132,837

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Hormonal Dynamics and Extracellular Vesicle Function in Keratoconus: Exploring Pathophysiology and Developing Targeted Therapies

Award Number: K99EY037781

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2028

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