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Metabolic regulation of neutrophil function

Award Number: F31HL186605
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 01/15/2027
PERIOD OF PERFORMANCE END DATE: 01/14/2028

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Metabolic regulation of neutrophil function - Project Summary Cardiac repair following myocardial infarction (MI) depends on a tightly regulated inflammatory response that clears necrotic tissue and promotes scar formation. Neutrophils are the first immune cells to infiltrate the injured myocardium and are essential for wound healing; however, excessive or prolonged neutrophil activation exacerbates tissue damage and contributes to adverse remodeling. Upon activation, neutrophils recruit and coordinate several effector functions, including production of reactive oxygen species (ROS), release of granular proteases, extrusion of neutrophil extracellular traps (NETs), and secretion of proinflammatory cytokines. Although these neutrophil effector functions likely evolved to improve chances of survival due to infection, such hypervigilant responses could be deleterious for tissue repair after sterile injuries, such as MI. Because neutrophils are terminally differentiated and have a short lifespan, they have a limited ability to regulate their responses via gene transcription. Instead, neutrophils exploit metabolic control mechanisms to coordinate and fine-tune their responses to tissue infection or injury. Although activation of the oxidative pentose phosphate pathway and glycolysis are known to be essential for effector functions such as the respiratory burst and for providing cellular energy, it is likely that neutrophils leverage other forms of metabolic control to titrate the nature and extent of their response to tissue damage. Our preliminary data reveal that activated neutrophils recruit the glycerol 3-phosphate (G3P) shuttle to sustain mitochondrial membrane potential and to promote ROS formation, which is important for effector functions such as NETosis. Accordingly, we propose that the neutrophil G3P shuttle contributes to a hyperinflammatory response after MI by promoting mitochondrial ROS formation, which is essential for NET release and intensifies immune cell recruitment, prolongs inflammation, and promotes excessive fibrosis, thereby contributing to excessive fibrosis and ventricular dilation. To test this hypothesis, we will: (1) determine how the G3P shuttle influences neutrophil effector function; and (2) elucidate the impact of the neutrophil G3P shuttle on ventricular inflammation and remodeling after MI. Collectively, this work will uncover fundamental metabolic mechanisms that regulate neutrophil responses to injury and define their impact on cardiac repair. These insights may inform new therapeutic strategies to optimize inflammation and resolution and improve post-MI outcomes. As a training vehicle, the techniques and strategies in this project will catalyze my development, providing knowledge and expertise essential for the development of an independent career in research.


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 = $37,174 )
2026	2026	UNIVERSITY OF LOUISVILLE	2301 S 3RD ST	LOUISVILLE	KY	40208	JEFFERSON	USA	Cardiovascular Diseases Research	000	1	7/20/2026	NEW	$37,174
														Subtotal = $37,174

Grand Total All Awards = $37,174

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Metabolic regulation of neutrophil function

Award Number: F31HL186605

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 01/15/2027

PERIOD OF PERFORMANCE END DATE: 01/14/2028

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