Funding

R01HL171984-01
Qyang (PI) - 12/01/2023 – 11/30/2027
NIH/NHLBI
Readily Available Biological Conduits to Treat Single Ventricle Defects This proposal is aimed at developing readily available biological conduits using cardiomyocytes, cardiac fibroblasts, and endothelial cells derived from hypoimmunogenic, universal human induced pluripotent stem cells (hiPSCs) coupled with acellular vascular scaffolds for the treatment of children born with single ventricle congenital heart defects (SVCHDs).

25IPA1454998
Qyang (PI) - 07/01/2025 – 06/30/2027
American Heart Association
Mitigation of Cardiac Fibrosis Using CAR-NK
This proposal aims to develop chimeric antigen receptor (CAR)-natural killer (NK) cell therapy to prevent myocardial fibrosis that causes tissue stiffness and heart failure, thus restoring myocardial contractile function.

1452253
Qyang (PI) - 07/01/2025 – 06/30/2028
Additional Ventures
Dynamic Training on Enhancing Endothelial Function and Cardiac Contractility of Biological Conduits
This study investigates the molecular mechanisms by which shear flow, mechanical, and electrical trainings rescue cardiac contractile and endothelial defects in single-ventricle patient-derived biological conduits.

R21AI194864
NIH/NIAID
Preclinical Pluripotent Stem Cell Investigation for Vascular Therapeutics
Qyang (PI) - 06/01/2026 – 05/31/2028
The purpose of this grant is to establish a porcine pluripotent stem cell model for preclinical investigation of stem cell-based regenerative therapy for patients who needs vascular graft replacement.

R01HL163092
Campbell (PI; Qyang co-I) - 04/15/2023 - 03/31/2027
NIH/NHLBI
Desmoplakinopathies: Integrated Pathophysiology and Therapeutics
Arrhythmogenic Cardiomyopathy (ACM) is a familial disease characterized by early-onset ventricular arrhythmias arising in the absence of overt cardiac remodeling of either structure or function, with subsequent emergence of mechanical dysfunction. This application focuses on uncovering mechanisms by which a mutation in the intercalated disc protein desmoplakin causes the full spectrum of ACM pathology including risk of exercise induced arrhythmia and heart failure. We will develop next generation therapies by targeting the upstream signaling cascade that causes this inherited disease.

R01HL136590
Campbell (PI; Qyang co-I) - 07/01/2023 - 06/30/2027
NIH/NHLBI
In this project, we will build a computational pipeline to predict the effects of mutations in tropomyosin and its binding partners troponin I and troponin T on cardiac function. The specific aims are: (1) Test the mechanistic validity of the model pipeline using rationally designed mutations, (2) Establish thresholds of pathogenicity using clinically established mutations, and (3) Test the ultimate ability of the model pipeline to identify pathogenicity of novel variants.

24CDA1051180 (Career Development Award)
Riaz (PI; Qyang as Faculty Sponsor - 04/01/2024 – 03/31/2027)
American Heart Association
Mechanistic Investigations of Amyloid Cardiomyopathy for Therapeutics Discovery
The overall objective is to investigate heart defects due to TTR amyloid cardiomyopathy.

25PRE1411217 (Predoctoral Award)
Yinsheng Lu (PI; Qyang as Faculty Sponsor - 01/01/2025 – 12/31/2026)
American Heart Association
A Wireless, Battery-Free, Miniatured Pacemaker for Tissue-Engineered Pulsatile Conduit Modulation The overall objective is create a new treatment that helps the heart work more like it should and reduces the need for additional surgeries.

26PRE1563816 (Predoctoral Award)
Qinzhe Xing (PI; Qyang as Faculty Sponsor - 01/01/2026 – 12/31/2027)
American Heart Association
Endothelialized Vascular Conduit as Arteriovenous Grafts
The overall objective is to create a new kind of tube that has a layer of protective cells inside, just like real blood vessels, to prevent blockage.

26PRE1569187 (Predoctoral Award)
Saba Fooladi (PI; Qyang as Faculty Sponsor - 01/01/2026 – 12/31/2027)
American Heart Association
Universal iPSC-CAR-NK Cells for Treatment of Fibrotic Heart Disease
The overall objective is to develop a new treatment that targets the cells that cause fibrosis due to the treatment of Ang II and phenylephrine in the heart.