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Deciphering neuronal circuits that mediate excessive sympathetic activation in heart disease

Award Number: F32HL188764
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 03/04/2027
PERIOD OF PERFORMANCE END DATE: 03/03/2028

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Deciphering neuronal circuits that mediate excessive sympathetic activation in heart disease - PROJECT SUMMARY Heart disease is the leading cause of death worldwide. Over 900,000 people each year in the U.S.—34 each minute—die from heart disease. The brain-heart axis, a complex network of bidirectional neural pathways, tightly regulates cardiac function, and its dysregulation is a major contributor to heart disease. Studying this axis offers the potential to uncover previously unrecognized mechanisms and to reveal novel therapeutic targets for many cardiac conditions. A key component of this axis, the sympathetic nervous system, mediates the body’s “fight-or-flight” response. After myocardial infarction, persistent and excessive sympathetic activation drives adverse cardiac remodeling, heart failure, and arrhythmias. To date, studies have largely assumed that sympathetic neurons are a uniform population and behave similarly. The possibility that diverse subtypes exist and that they may have organ-specific functions has not yet been explored. Thus, standard heart disease drugs target only one of the many signaling molecules released by sympathetic neurons. This approach has likely masked important effects of distinct sympathetic neuron subtypes on health and disease. Recent single-cell transcriptomic data from the sympathetic ganglia have identified distinct neuronal subtypes, including one that highly expresses neuropeptide Y (NPY) and another that expresses its receptor, NPY2R. NPY is strongly implicated in heart disease, yet the mechanisms by which it drives adverse remodeling remain poorly understood. Our preliminary data identify a population of NPY2R neurons in the sympathetic ganglia, distinct from NPY neurons. Viral tracing demonstrates dense innervation of the heart, and selective activation of these neurons increases heart rate. However, their physiological role and interaction with NPY neurons in disease remain unknown. We hypothesize that a feedforward circuit exists between NPY and NPY2R neurons in the sympathetic ganglia, in which NPY release after cardiac injury recruits NPY2R neurons through an endocrine-like signaling mechanism. This would amplify sympathetic tone, prompting heart failure and arrhythmias. Using a combination of viral tracing, cell-type-specific manipulation, and in vivo physiological recordings, we will anatomically map and characterize the function of NPY2R neurons in health (Specific Aim 1) and after myocardial infarction (Specific Aim 2) in a mouse model. Validating this pathway could uncover novel targets for more precise therapeutics and lay the foundation for translational studies to improve outcomes for patients with heart failure and life-threatening arrhythmias.


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 = $87,148 )
2026	2026	UNIVERSITY OF CALIFORNIA, LOS ANGELES	10889 WILSHIRE BLVD STE 700	LOS ANGELES	CA	90024	LOS ANGELES	USA	Cardiovascular Diseases Research	000	1	9/4/2026	NEW	$87,148
														Subtotal = $87,148

Grand Total All Awards = $87,148

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Deciphering neuronal circuits that mediate excessive sympathetic activation in heart disease

Award Number: F32HL188764

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 03/04/2027

PERIOD OF PERFORMANCE END DATE: 03/03/2028

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