NIH-funded research R01 grant

Investigating how stiffening of the aorta from elastin loss causes SVAS

Official title: Investigating altered smooth muscle cell mechanotransduction as a cause of supravalvular aortic stenosis

Funded at Utah State Higher Education System--University of Utah · NIH-11568641 · Data updated 2026-11-12

A new NIH grant is exploring why elastin loss leads to supravalvular aortic stenosis and how abnormal smooth muscle cell signaling causes the aorta to narrow in children.

More Aortic Stenosis research and trials

Quick facts

Grant typeR01 grant
Study typeNIH-funded research
Funding institutionUtah State Higher Education System--University of Utah
NIH-funded
Lab location1 site (Salt Lake City, United States)
Project startDecember 1, 2022
Project endNovember 30, 2027
Funding year2026
Award (this year)$217,671
NIH project number7R01HL166448-05
Project IDNIH-11568641 on NIH RePORTER

Who could benefit from this research

Could help

Children and young adults with or at risk for supravalvular aortic stenosis due to elastin-related mutations may benefit from insights that guide future treatments.

Less likely to help

People without SVAS or elastin-related conditions may not benefit from this basic mechanistic research.

What this research studies

This project studies SVAS, a condition where the aorta narrows due to elastin gene mutations, by looking at how mechanical changes affect smooth muscle cells in the aorta. Researchers will examine mechanosensitive channels like Piezo1/2 and their role in calcium signaling and nuclear regulation that may drive cell changes leading to narrowing. Using a targeted mouse model that mimics human elastin deficiency, the team will track how reduced aortic stiffness alters cell behavior and gene expression related to cell differentiation and proliferation. The goal is to uncover actionable mechanisms that could be targeted with future therapies to prevent or lessen SVAS in affected patients.

Why it matters

Potential benefit: If successful, the findings could point to new therapeutic strategies to prevent or reduce aortic narrowing in SVAS patients.

How similar studies have gone: Preliminary data in a mouse SVAS model show mechanistic links between elastin insufficiency, altered aortic stiffness, and SMC signaling, supporting potential relevance to humans.

Where this research is happening

  • Utah State Higher Education System--University of Utah
    Salt Lake City, United States
    Active

Researchers

  • Principal investigator: Wagenseil, Jessica — Utah State Higher Education System--University of Utah
  • Study coordinator: Wagenseil, Jessica

Related research

Other NIH-funded projects on the same topics.

About this research

  1. This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
  2. Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
  3. For full project details, budget, and progress reports, visit the official NIH RePORTER page.
Last reviewed 2026-11-14 by the Find a Trial editorial team. Information on this page is for educational purposes and is not medical advice. Always consult qualified healthcare professionals about clinical trial participation.