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Elucidating the impact of ADAMTS7 on Coronary Artery Disease

Award Number: F31HL184820
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/01/2026
PERIOD OF PERFORMANCE END DATE: 11/30/2027

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Elucidating the impact of ADAMTS7 on Coronary Artery Disease - PROJECT SUMMARY Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death in the Western world, affecting approximately one in three adults. Despite advances in lipid-lowering therapies, ASCVD prevalence continues to rise, highlighting an urgent need for novel therapeutic strategies targeting underlying disease mechanisms. Human genome-wide association studies consistently link ADAMTS7, encoding a matrix metalloproteinase, to ASCVD, but the precise mechanisms through which ADAMTS7 contributes to disease pathogenesis remain unclear. Previous studies indicate Adamts7 promotes vascular smooth muscle cell (VSMC) migration and neointimal formation, suggesting an influential role in atherosclerosis. Recent findings demonstrate that VSMC-specific Adamts7 overexpression promotes the emergence of a foamy VSMC subpopulation within atherosclerotic lesions due to increased lipid uptake by the VSMCs. This foamy subset notably exhibits upregulated expression of the transcription factor Spi1, implicating Spi1 as a potential downstream mediator of Adamts7-driven cellular transitions during atherogenesis. Building directly upon these findings, this project aims to define the mechanisms by which Adamts7 influences VSMC phenotypes and promotes ASCVD and the role of Spi1 in this process. I will assess whether Spi1 mediates the proatherogenic effects of Adamts7. Mice with VSMC-specific Adamts7 overexpression and Spi1 knockout will be evaluated for changes in lesion size, VSMC foam cell formation, and inflammatory responses. Then, I will characterize Adamts7-driven transcriptional and epigenetic changes in vascular cells during atherosclerosis using single-nucleus multiome sequencing (snMultiome-seq). The analysis will identify cell-type specific gene regulatory networks altered by Adamts7 overexpression, focusing on chromatin changes near Spi1 locus. All key findings will be validated in mouse and human vascular tissues through RNAscope and immunohistochemistry, addressing discrepancies regarding ADAMTS7’s role in human disease. Collectively, this work will provide novel insights into ADAMTS7-mediated mechanisms of ASCVD, potentially informing new therapeutic interventions targeting VSMC modulation. Overall, this proposal includes comprehensive training in ASCVD genetics, experimental models, and advanced genomic technologies, conducted within a supportive research environment, fostering my development toward an independent scientific career.


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 = $50,114 )
2026	2026	THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK	630 W 168TH ST FL 4	NEW YORK	NY	10032	NEW YORK	USA	Cardiovascular Diseases Research	000	1	5/20/2026	NEW	$50,114
														Subtotal = $50,114

Grand Total All Awards = $50,114

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Elucidating the impact of ADAMTS7 on Coronary Artery Disease

Award Number: F31HL184820

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/01/2026

PERIOD OF PERFORMANCE END DATE: 11/30/2027

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