Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( 🔒 ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Need Help

SNAP23 is a Novel Regulator of Autophagy in Cardiac Myocytes

Award Number: F31HL182196
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/23/2026
PERIOD OF PERFORMANCE END DATE: 12/22/2027

Group Awards By:

View Award Description

SNAP23 is a Novel Regulator of Autophagy in Cardiac Myocytes - Project Summary Heart disease is the leading cause of mortality in the US and is often preceded by pathological cardiac hypertrophy due to chronic hypertension and sustained increases in cardiac afterload. While initially an adaptive response to maintain cardiac output and systemic blood supply, pathological cardiac hypertrophy eventually leads to a decompensated state of heart failure (HF). The initial adaptive aspect of hypertrophic growth requires increases in protein synthesis, which must be balanced by adequate protein folding, and degradation of misfolded, potentially toxic proteins. Without this balance, cardiac myocytes cannot maintain protein homeostasis, or proteostasis, which threatens functional cellular integrity and viability. Autophagy is a highly conserved mechanism that is critical for maintaining cardiac myocyte proteostasis via its capacity to eliminate dysfunctional cellular components and potentially toxic protein aggregates. Despite being highly dependent on a series of membrane fusion events that are rate limiting steps in regulating autophagy, the function of soluble NSF attachment protein receptor (SNARE) proteins that mediate these steps remain poorly understood in the heart. In this proposal, we will investigate novel regulatory roles for the SNARE protein, synaptosomal-associated protein 23 kDa (SNAP23), with the Hypothesis that SNAP23 is required for cardiac myocyte autophagy as a means to preserve cardiac function in response to pressure overload-induced cardiac hypertrophy. Our preliminary data employed molecular approaches to enable SNAP23 loss- and gain-of-function in primary cardiac myocytes where we assessed the efficiency of autophagy (i.e. autophagic flux) via treatment with the lysosomal inhibitor, bafilomycin A1. We observed that while SNAP23 loss-of-function decreased autophagic flux, SNAP23 gain-of-function increased autophagic flux under both basal and stress-induced conditions. We subsequently performed immunoprecipitation experiments and identified key autophagy proteins as functional interacting partners with SNAP23 in cardiac myocytes. Finally, we generated cardiac-specific SNAP23 knockout mice (SNAP23cKO) which resulted in pathological cardiac remodeling and dysfunction that was associated with impaired autophagy. Here, we propose to extend upon our preliminary findings and address our hypothesis using cardiac-specific targeting of SNAP23 in mice as well as mechanistic studies in primary cardiac myocytes isolated from the adult mouse heart in the following Specific Aims which are to: (Aim 1) determine the effects of SNAP23 loss- and gain-of-function on cardiac myocyte autophagy, and (Aim 2) examine the effects of SNAP23 gain-of- function on cardiac structure, function, and autophagy in response to pressure overload-induced cardiac hypertrophy. These studies are significant because they will address the current knowledge gap regarding functional roles for SNARE proteins in the heart with a specific focus on SNAP23 as a regulator of cardiac myocyte autophagy. They will also examine whether ectopic expression of SNAP23 can protect against pressure overload-induced cardiac hypertrophy via mediating autophagy.


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 = $40,799 )
2026	2026	UNIVERSITY OF UTAH	201 PRESIDENTS CIR	SALT LAKE CITY	UT	84112	SALT LAKE	USA	Cardiovascular Diseases Research	000	1	6/30/2026	NEW	$40,799
														Subtotal = $40,799

Grand Total All Awards = $40,799

Top

All Categories

About

Search

Reports

Data Submission

Award Information

SNAP23 is a Novel Regulator of Autophagy in Cardiac Myocytes

Award Number: F31HL182196

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/23/2026

PERIOD OF PERFORMANCE END DATE: 12/22/2027

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer