Cardiovascular T32 Training Program
SEPT 3 📢: LHI Welcomes new T32 Co-Director Xavier Revelo, PhD!
Bridging the Gap from Concept to Clinical Reality
The University of Minnesota’s T32 Training Program offers a premier interdisciplinary environment dedicated to the next generation of cardiovascular innovators. Our mission is to equip trainees with the tools to navigate the entire lifecycle of medical discovery—from the initial conceptual spark to rigorous testing in basic, animal, and human models.
Why Choose Our Program?
We leverage the combined power of the Lillehei Heart Institute, the U of M Cardiovascular Division, and the Twin Cities’ world-renowned biotech and medical device ecosystem.
- Dual Focus: Gain deep expertise in CV science paired with formal entrepreneurship training.
- Industry Integration: Benefit from direct industry mentorship, supported business externships, and meaningful networking within the local pharma and device sectors.
- Academic Excellence: Access world-class curriculum through the Carlson School of Management (MILI) and the College of Science and Engineering (TLI)
Core Research Pillars
Our program centers on three specialized focus areas:
- Regenerative Medicine
- Arrhythmias and Resuscitation Science
- Muscle Physiology
The Trainee Experience: Beyond the Lab
We provide more than just a research seat; we provide a career launchpad. Unique features of our curriculum include:
- Business Mastery: Dedicated time for business plan development and grant writing.
- The "Shark Tank" Experience: Pitch your innovations in a high-stakes, constructive environment.
- Tailored Mentorship: Guidance from highly qualified trainers and active industry leaders.
Inquiries may be made via email to the Program Director, Dr. Samuel Dudley, [email protected].
Nora Ahmed
Started T32 in 2026
Research:
My current research focuses on elucidating the molecular mechanisms that regulate protein stability in cardiac muscle disease, using human iPSC-derived cardiac myocytes (hiPSC-CMs) and animal models. I am investigating how microdystrophin (micro-Dys), the truncated therapeutic transgene delivered by AAV in Duchenne muscular dystrophy (DMD) gene therapy, is targeted for rapid degradation, with a particular focus on the muscle-specific ubiquitin-proteasome axis that act to destabilize it. Using post-translational modification mapping, computational variant design, and CRISPR-based screens, I am working to engineer more stable µDys variants and validate them, with the goal of closing the gap that currently limits DMD gene therapy outcomes.
Parallel efforts are directed toward a hiPSC-CM model of cancer cachexia-induced cardiomyopathy, where I am mapping how FOXO-driven transcriptional programs and mTORC1 suppression converge to drive contractile decline and protein wasting in the cardiac myocyte. In the longer term, I am interested in integrating these mechanistic insights across disease contexts to develop therapeutic strategies that stabilize essential cardiac proteins and halt the progression of structural and functional decline in genetic and metabolic heart disease.
Publications:
- Hosny, Nora, Houda Cohen, John Bauer, Jeff Schreifels, Rachel Lin, Brian R. Thompson, and Joseph M. Metzger. “Engineering Human Myocardium: Integrating the Maturation of hiPSC-Derived Cardiac Myocytes Across Genetic, Structural, Physiological and Multicellular Systems.” Cells 15, no. 11 (2026): 1019.
Upendra Chalise
Started T32 in 2024
Research:
Identifying the role of neutrophils in cardiac pressure overload. My project is examining the role of neutrophils in initiating the early inflammatory milieu in the left ventricle with the pressure overload following transaortic constriction surgery. I am interested in understanding the temporal abundance and changes in heterogeneity of neutrophils in the left ventricle and periphery following the cardiac injury. Neutrophils are known to directly regulate adverse cardiac remodeling and cardiovascular deaths in ischemic cardiac injury and my project is identifying how it affects the same in a non-ischemic injury as it is completely unknown in the field. I am studying how depletion of neutrophils or deletion of specific inflammatory components in neutrophils directly affects adverse cardiac remodeling in the left ventricular pressure overload.
Publications: (since starting on the T32 in 2024)
- Yücel D, Smith C, Ferreira de Araujo N, Souza-Neto F, Chalise U, Schuler G, Garay BI, Mikkila JL, Mahmoud OAA, Mandal P, Perlingeiro RCR, van Berlo JH. Small-scale siRNA screen reveals WWC2 as a novel regulator of cardiomyocyte mitosis. J Mol Cell Cardiol. 2026 Jan;210:127-136. doi: 10.1016/j.yjmcc.2025.11.004. Epub 2025 Nov 15. Erratum in: J Mol Cell Cardiol. 2026 Feb;211:131. doi: 10.1016/j.yjmcc.2025.12.007. PMID: 41248802; PMCID: PMC12853299.
- Parthiban P, Barrow F, Wang H, Chalise U, Araujo N, Souza-Neto F, Nguyen H, Draxler M, Pallais JP, Yucel D, Liu H, Ciske E, Fehrenbach P, Hakeem A, Lee SH, Herman A, Rothenberg ME, Dudley S, van Berlo JH, Revelo XS. Macrophage-Derived CCL24 Promotes Cardiac Fibrosis Via Fibroblast CCR3. Circ Res. 2025 Oct 10;137(9):1140-1156. doi: 10.1161/CIRCRESAHA.125.326599. Epub 2025 Sep 16. PMID: 40955564; PMCID: PMC12509456.
Scientific Presentations:
- Chalise U, Gaire A, Shen S, van Berlo JH. Macrophages regulate fibroblasts to coordinate fibrosis after cardiac pressure overload. American Society for Matrix Biology Biennial Meeting 2025. (Oral Talk, finalist for Iozzo Postdoc Award)
- Chalise, U, Souza-Neto F, Gaire A, Shen S, van Berlo JH. Padi4 deletion prevents adverse cardiac remodeling and heart failure progression during cardiac pressure overload. Journal of Molecular and Cellular Cardiology, International Society for Heart Research Congress, 2025. (Poster Presentation)
Fellowships or other support:
- UMN Presidential Fellowship
Gyeoung-Jin Kang
Started T32 in 2024
Research:
My current research focuses on elucidating the molecular mechanisms that regulate cardiac ion-channel mRNA stability and on pathways that resolve inflammation in diabetic cardiomyopathy. I am investigating how alternative splicing events and dysregulation of RNA-binding proteins converge to suppress SCN5A expression in cardiomyopathic myocardium, as well as how non-coding RNAs destabilize SCN5A transcripts and attenuate sodium current. Parallel efforts are directed toward understanding inflammatory signaling in diabetic cardiomyopathy, with the goal of identifying molecular pathways whose modulation can resolve chronic inflammation and improve cardiac outcomes. In the longer term, I am interested in integrating these mechanistic insights to develop novel therapeutic approaches aimed at reducing arrhythmogenic vulnerability and halting the progression of cardiomyopathy.
Publications: (since starting on the T32 in 2024)
- M Liu, H Liu, EJ Kim, GJ Kang, M Neumann, M Johnson, R Murikinati, and SC Dudley: “Dapagliflozin Prevents Diabetic Heart Failure With Preserved Ejection Fraction by Inhibiting the Sodium/Hydrogen Exchanger”, JACC: Basic to Translational Science, Accepted, 2026 Aug.
GJ Kang, EJ Kim, A Xie, H Liu, and SC Dudley: “Stress-Induced Down-Regulation of CPEB4 Disrupts Sodium Channel Regulation and Myocardial Excitability”, JACC: Basic to Translational Science, 11(4):101514, 2026 Mar. - A Xie, GJ Kang, H Liu, EJ Kim, D Dobrev, and SC Dudley: “Lysosomal Ca2+ Release Through TRPML1 Governs Ventricular Arrhythmia After Myocardial Infarction”, Circulation: Arrhythmia and Electrophysiology, 14:e013964, 2025 Nov. Co-first authorship.
- M Liu, H Liu, GJ Kang, LM Hartweck, F Feng, EJ Kim, KW Prins, and SC Dudley: “Cardiac TRPM7 Causes Diabetic Heart Failure With Preserved Ejection Fraction”, JACC: Basic to Translational Science, 10(8):101321, 2025 Aug.
- A Xie, GJ Kang, EJ Kim, H Liu, F Feng, and SC Dudley: “C-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy”, Circulation: Arrhythmia and Electrophysiology, 17(10):e013054, 2024 Oct. Co-first authorship.
Manuscripts Submitted/In Preparation:
- M Liu, H Liu, Arujo N, EJ Kim, GJ Kang, M Neumann, R Murikinati, M Johnson, van Berlo J, and SC Dudley: “The role of macrophage TRPM7 kinase in hypomagnesemia-induced heart failure with preserved ejection fraction”, Journal of the American Heart Association, Under Revision, 2026 Aug.
- GJ Kang, A Xie, EJ Kim, and SC Dudley: “Loss of the Stress-Responsive lncRNA LINC00667 Drives SCN5A Decay and Arrhythmia Susceptibility in Heart Failure by Altering mRNA Stability”, Circulation: Arrhythmia and Electrophysiology, Submitted, 2026 Aug.
- H Choi, GJ Kang, EJ Kim, Y Guo, H Liu, and SC Dudley: “Cardiac 5-LOX/RvD1 Pro-Resolving Signaling Improves Diabetic Heart Failure With Preserved Ejection Fraction”, JACC: Basic to Translational Science, Submitted, 2026 Sep. Co-first authorship.
Scientific Presentations:
- GJ Kang: “A Patent-Backed miR-448 RNA Strategy to Restore Cardiac Electrical Reserve,” Shark Tank Competition Oral Presentation, Cardio Palooza 17, University of Minnesota, July 2026.
- GJ Kang, EJ Kim, A Xie, and SC Dudley: “Stress-Induced Regulation of SCN5A Alternative Splicing by LINC00667 and RBM5 in Human Cardiomyocytes”, Poster Presentation, International Society for Heart Research North American Section (ISHR-NAS), 2026 May.
- GJ Kang, EJ Kim, A Xie, and SC Dudley: “Regulation of SCN5A Alternative Splicing by LINC00667 in Human Cardiomyocytes”, American Heart Association Scientific Sessions 2025, 2025 Nov. (Circulation. 152(Suppl_3):4370654).
Intellectual Property:
- Samuel Dudley, GJ Kang, and EJ Kim: “Gene Therapy for HFpEF”, University of Minnesota Invention Disclosure, UMN 2025-004, 2025.
- Samuel Dudley, GJ Kang, and EJ Kim: “Gene Therapy for Acquired Arrhythmia”, University of Minnesota Invention Disclosure, UMN 2025-003, 2025
Coursework completed:
LNS X001 - 034 Intro to Research Commercialization.
Grant Applications:
- Principal Investigator — NIH R01: “mRNA Instability and Arrhythmias.” Initial application submitted, 2025 Oct; resubmission planned, 2026 Nov.
- Principal Investigator — AHA CDA: “CPEB4-Directed RNA Networks in Atrial Electrical Remodeling and Fibrillation.” Application prepared for the 2025 Dec cycle but not submitted; submission planned, 2026 Dec.
- Scientific Lead — NIH R01: “Long Noncoding RNA, the Unfolded Protein Response, and Arrhythmia.” A1 resubmission submitted, 2026 Mar; revised new application planned, 2026 Oct.
- Scientific Lead — DoD PRMRP: “Therapy for Hypoxic Arrhythmias.” Newly developed project; initial application submitted, 2026 Jul.
- Contributing Investigator — NIH R01: “Modulation of Inflammation to Treat Diastolic Dysfunction.” Resubmission planned, 2026 Oct.
Cutler Lewandowski
Started T32 in 2025
Research:
My current research focuses on cardiomyopathy associated with Duchenne muscular dystrophy (DMD). I am utilizing human induced pluripotent stem cells (iPSCs) to generate cardiomyocytes and other cell types that enables complex, three-dimensional modeling of this cardiomyopathy. In these models, we can evaluate phenotypic differences among individuals with DMD-associated cardiomyopathy and assess the cardiac response to emerging therapeutics for DMD. In my future research, I hope to employ this innovative and translational precision medicine approach to develop new DMD therapies and match patients with DMD-associated cardiomyopathy to the most appropriate and effective treatments.
Former Trainees
Sasha Prisco, MD, PhD
Sasha Prisco, MD, PhD
Education/Credentials
MD, Medicine, Medical College of Wisconsin
PhD, Physiology, Medical College of Wiconsin
Trainee 2019-2022
Mentor: Kurt Prins, MD, PhD
Research Project Area/Focus:
Investigating the Role of the Intestinal Micro- and Mycobiome in Pulmonary Hypertension
Accomplishments:
Clinical and Translational Science Institute (CTSI) Translational Research Development Program Grant (2020-22)
Physician-Scientist Training Program (PSTP) Academic Investment in Education Grant (received each year over four consecutive years) (2019-23)
Cardiovascular Retreat (Cardio Palooza) Best Fellow Poster Award (2019)
Northwestern Cardiovascular Young Investigators’ Forum Winner in Fellows Basic Science (2020)
National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award (T32 Grant) (2019-21)
Northwestern Cardiovascular Young Investigators’ Forum Finalist in Fellows Basic Science (2019)
Anthony Prisco, MD, PhD
Anthony Prisco, MD, PhD
Trainee 2019-2021
Mentor: Paul Iaizzo, PhD
Research Project Area/Focus:
Dr. Prisco was a cardiovascular diseases fellow and engineer with a strong interest in using mathematical modeling to better understand cardiovascular disease, develop better treatments, and improve patient care. Currently, he has two main research foci: computational fluid dynamics and artificial intelligence. He uses computational fluid dynamics to model complex blood flow in heart valves and cardiopulmonary bypass machines. Additionally, he is developing mathematical techniques to predict if valves placed percutaneously will leak following implantation. In cardiopulmonary bypass, he is working on better understanding how patients with multisystem organ failure maintain end-organ oxygenation while on bypass. Finally, he is currently using convolutional neural networks, a type of artificial intelligence, to diagnose subclinical cardiovascular disease in high-risk patients.
Accomplishments:
University of Minnesota: Anthony Garofalo Prevention Fellowship Award 2021
Victoria Osinski, MD, PhD
Victoria Osinski, MD, PhD
Education/Credentials
PhD, Experimental Pathology, Biomedical Sciences Graduate Program, University of Virginia
Trainee 2020-2022
Mentor: Bryce Binstadt, MD, PhD
Research Project Area/Focus:
Dr. Osinski's research involved two projects focused on improving the understanding of the role that stromal and vascular cells play in response to chronic inflammation in the mitral valves. These studies examined specific cellular processes and signaling molecules that are believed to be relevant to the mechanisms driving pathologies observed in rheumatic heart disease and other forms of endocarditis. To study this, she employed the use of the transgenic mouse model of arthritis K/B.g7 in which the mouse generates autoantibodies that prompt inflammation and fibrosis in the joints as well as the heart. Project 1 specifically focused on characterizing the lymphatics in the mitral valves of these mice and determining whether they promote or inhibit disease progression early on and later in valve inflammation. Her specific hypothesis was that lymphangiogenesis inhibits disease early on, but later promotes it. This project was motivated by data identifying new vascular structures in inflamed valves of K/B.g7 mice using cre-lox recombination lineage-tracing driven by the endothelial-specific Cdh5 promoter. These identified vessels express lymphatic markers VEGFR3 and LYVE1. Project 2 aimed to understand whether expression of IL4Rɑ in fibroblasts promotes valve inflammation and fibrosis. Previous work from the laboratory demonstrated that macrophage-produced IL-13 drives valve inflammation, but it remains unclear which cell types bind and respond to this cytokine to induce this pathology. She hypothesized that loss of IL4Rɑ in fibroblasts would protect against IL-13-driven valve inflammation and fibrosis. Both projects employed the use of cell-specific gene knockout murine lines, flow cytometry and histology assays, and human mitral valve samples to validate the presence of important cell types and proteins in patients with rheumatic disease and other inflammatory heart diseases. Since the mitral valve samples are obtained from deidentified, discarded tissue, this is not considered human research.
Daphne Moutsoglou, MD, PhD
Daphne Moutsoglou, MD, PhD
Education/Credentials
MD, University of Colorado Anschutz Medical Campus
PhD, Immunology, University of Colorado Anschutz Medical Campus
Trainee 2020-2023
Mentor: Thenappan Thenappan, MD
Research Project Area/Focus:
Daphne Moutsoglou, MD, PhD is a gastroenterology fellow at the University of Minnesota. She completed her PhD in immunology and MD in the combined Medical Scientist Training Program at the University of Colorado. At this time, her goals are to continue to conduct research in academia studying the interaction between the microbiome and immune system in disease. Under the Cardiology T32 training grant, she studied the role of the microbiome in pulmonary arterial hypertension (PAH) as well as the role of microbiota transplant therapy (previously known as fecal microbiota transplant) in two clinical trials, one in PAH and ulcerative colitis.
She has conducted a separate descriptive study of human microbiota in PAH and has found that the fecal microbiomes of PAH patients are different from healthy and family controls (those that cohabitate with patients with PAH). She has also found differences in gut microbial metabolites using targeted metabolomics. These data have been published.
Additionally, she has taken these findings and applied to the FDA, for an investigational new drug (IND) application (IRB# STUDY00012951, CT.gov#: NCT 04884971). During her time on this project, she has written the investigational new drug application to the FDA, submitted it, and communicated with the FDA regarding revisions to get its final approval. She has also completed the clinical trial and is currently analyzing the results.
To complete this analysis, she collected stool samples from trial patients and is testing for engraftment of fecal microbiota. She is also analyzing blood from patients in the trial to look for markers of disease and changes in microbial metabolites.
She also completed an in vivo project studying the rat microbiome and effects of intermittent fasting in a monocrotaline rat model of pulmonary arterial hypertension. These data have been published.
She has also been working as Co-PI on another randomized, double-blinded placebo controlled clinical trial studying microbiota transplant therapy and engraftment in ulcerative colitis patients at the University of Minnesota and an additional trial studying fecal microbiota transplant in post-operative Crohn’s disease patients. She is currently completing the microbiome analysis for these trials.
Accomplishments:
First Prize, 2021 ATS Conference BEAR Cage Competition, ATS International Conference, 2021 American Journal of Respiratory and Critical Care Medicine Emerging Investigator, March 2023
June Baik, PhD
June Baik, PhD
Trainee 2021-2022
Mentor: Rita Perlingeiro, PhD
Research Project Area/Focus:
Establishment of a non-human primate myogenic model for enabling cell-based therapy for muscle degenerative disorders. Transplanting pluripotent stem cell-derived (PSC) myogenic progenitors in a large animal model is critical to evaluate feasibility of cell-based therapies for muscular dystrophy. To address this, 3 Macaca fascicularis iPS cell lines (Cy0657#5, CyMN.1 and CyMN.2) and applied conditional expression of PAX7, which resulted in robust in vitro myogenic differentiation. Whole transcriptome analysis of NHP-PSC cultures undergoing myogenic specification confirmed the successful sequential induction of mesoderm, paraxial mesoderm and myogenic lineages, respectively. Pilot in vivo studies with CyMN.2 Pax7-induced myogenic progenitors show that these cells contribute to muscle regeneration upon transplantation into cardiotoxin-injured muscles of immunocompromised mice. Testing in Macaca fascicularis recipients will provide insights to define key aspects associated with cell delivery in larger muscles and investigate the interaction between donor cells and the host immune system.
Accomplishments:
Travel Award for the 2021 Frontiers in Myogenesis Conference
Sarah Crist, MD, PhD
Sarah Crist, MD, PhD
Trainee 2022-2024
Mentor: Rita Perlingeiro, PhD
Research Project Area/Focus:
Exploring the dichotomous role of collagen deposition in iPSC-derived skeletal muscle and cardiac transplants
Characterizing how the adult environment impacts the maturation of human and mouse PSC-derived iPAX7/3 myogenic progenitors
Alex Dayton, MD, PhD
Alex Dayton, MD, PhD
Education/Credentials
MD, PhD, Medicine and Physiology, Medical College of Wisconsin
Trainee 2022-2024
Mentor: John Osborn, PhD
Research Project Area/Focus:
Renal denervation for prevention of tacrolimus-induced nephrotoxicity in rats
Accomplishments:
University of Minnesota Department of Surgery Research Week 2022, Second Prize, Clinical/Education Research Category
Patrick Ernst, MD, PhD
Patrick Ernst, MD, PhD
Education/Credentials
Ph.D. in Biomedical Engineering, University of Alabama at Birmingham
Trainee 2022-2025
Mentor: Forum Kamdar, MD, PhD
Research Project Area/Focus:
- Adrenergic Stress and SERCA Upregulation in Duchenne Muscular Dystrophy Cardiomyopathy
- Toward a 3D Human Model of Duchenne Muscular Dystrophy Cardiomyopathy
- Using patient-derived hiPSC-CMs to study mechanisms behind disease progression in DMD cardiomyopathy. A lot of focus is on calcium handling due to the high incidence of arrhythmias in these patients, we are also looking at mitochondrial function since there is little data on cardiac mitochondrial dysfunction in DMD and what there is is in mouse models that don't model the human cardiomyopathy very well. We have been working on incorporating bioprinting & 3D tissue engineering to generate more clinically relevant models, though that has been less of a focus lately as we have been working a lot on troubleshooting & improving that with the help of a newer lab member.
Accomplishments:
UMN Hebbel Research Day Poster Award (2024, 2025)
T32 Program Director
Samuel Dudley, MD, PhD
Professor of Medicine
Cardiovascular Division
University of Minnesota Medical School
T32 Program Co-Director
Xavier Revelo, PhD
McKnight Land Grant Professor of Immunometabolism
Department of Integrative Biology and Physiology
University of Minnesota Medical School
Cardiovascular T32 Training Program Inquiries
Inquiries about the Cardiovascular T32 Training Program may be made via email to the Program Director, Dr. Samuel Dudley, [email protected].
FELLOWSHIP PROGRAMS
SUBSPECIALTIES
Advanced Cardiovascular Imaging
Advanced Heart Failure & Transplant Cardiology
Clinical Cardiac Electrophysiology
Advanced Interventional Cardiology & Research
Internal Medicine Critical Care Medicine
Dual-Track: Advanced Heart Failure/Critical Care Medicine
Dual-Track: Critical Care Medicine/ Interventional Cardiology