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COMPLEMENT IN THE CELLULAR MICROENVIRONMENT DURING CARDIAC RENEWAL

Award Number: R00HL174827
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 08/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2029

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COMPLEMENT IN THE CELLULAR MICROENVIRONMENT DURING CARDIAC RENEWAL - PROJECT SUMMARY (See instructions): lschemic heart disease (IHD) is the leading cause of death worldwide, resulting in 9 million deaths yearly. Current treatments for IHD are medications or surgical procedures to improve blood flow, which cannot address the underlying permanent loss of cardiomyocytes (CMs) resulting from myocardial infarction (MI). After MI, the heart undergoes fibrotic repair rather than regeneration. This leads to maladaptive remodeling, further death of CMs, and eventual heart failure (HF) over time. In IHD patients with HF, heart transplant becomes the only therapy. However, new cases of HF far outpace the number of heart transplant procedures performed each year. Therefore, there is an urgent need for therapeutics that directly address the loss of CMs. In neonatal mammalian hearts post-MI and in adult hearts expressing active yes-associated protein 1 (YAP), a transcriptional co-regulator of cell proliferation, CMs can re-enter the cell cycle and divide to generate new CMs. I have uncovered that in both models, CM proliferation requires interplay between poised CMs, cardiac fibroblasts (CFs), and tissue-resident macrophages (MPs); poised CMs re-enter the cell cycle, while the Complement pathway, a component of innate immunity, is activated in CFs and MPs to facilitate CM cell cycle progression and de-differentiation. Specifically, C3 is activated in CFs and C3ar1 is activated in MPs, with C3 or C3ar1 knockout (KO) resulting in decreased CM proliferation. The central hypothesis of this proposal is activation of Complement alters the composition and metabolism of the cardiac microenvironment to promote CM proliferation. Aim 1 will investigate the direct role for C3ar1 MPs in CM proliferation through secreted factors and changes to the extracellular matrix. Aim 2 will study the function of C3 in CFs on the cardiac microenvironment in response to Ml. The proposed project will extend our understanding of in vivo CM proliferation and the various cell-cell interactions of the renewal competent niche. The mentored K99 phase has prepared me with the knowledge and tools needed to study cardiac renewal and complement signaling in the heart. The R00 phase will help me establish an independent research program at Temple University on cardiac regeneration, with a focus on the complement system and the microenvironment.


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 = $249,000 )
2026	2026	TEMPLE UNIVERSITY-OF THE COMMONWEALTH SYSTEM OF HIGHER EDUCATION	1805 N BROAD ST	PHILADELPHIA	PA	19122	PHILADELPHIA	USA	Cardiovascular Diseases Research	000	4	8/4/2026	EXTENSION WITH OR WITHOUT FUNDS	$249,000
														Subtotal = $249,000

Grand Total All Awards = $249,000

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COMPLEMENT IN THE CELLULAR MICROENVIRONMENT DURING CARDIAC RENEWAL

Award Number: R00HL174827

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 08/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2029

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