Research interests
C166 EVs potentiate miR cardiac reprogramming via miR-148a-3p[9]
Conrad Phillip Hodgkinson
Research Principal Investigator for an NHLBI-funded cardiac reprogramming project
As of 2029 · Last known relationship
Research Principal Investigator for an NHLBI-funded cardiac reprogramming project
As of 2029 · Last known relationship
Conrad Phillip Hodgkinson is a Duke University physician-scientist and principal investigator pursuing cardiac regeneration through cellular reprogramming. He studies how fibroblasts, which form scar tissue after heart injury, can be converted into cardiomyocytes, with recent work examining beta-catenin signaling, injured-heart factors, chromatin regulation, microRNAs, and extracellular-vesicle delivery. He is currently Associate Professor in Medicine and Associate Professor of Pathology at Duke, and leads an NHLBI-funded cardiac reprogramming project running from 2025 to 2029. Hodgkinson earned a Ph.D. from the University of London in 1996. Earlier Duke roles included Assistant Professor of Pathology, Assistant Professor in Medicine, and Medical Instructor in the Department of Medicine. His research has also addressed cardiac progenitor cells, paracrine mechanisms, aging, and gene and cell engineering for cardiovascular repair.
Each topic is linked to its supporting source in Sources.
Training includes Research Principal Investigator for an NHLBI-funded cardiac reprogramming project, Research Principal Investigator for the CTX340 AGT in vivo gene-editing collaboration awarded by CRISPR Therapeutics, Research Principal Investigator for a Rosenfeld Heart Foundation project on enhancing cardiac reprogramming through TLR3, and Ph.D. from the University of London, plus 7 more records.
Explore education and trainingAs of 2029
As of 2026
As of 2024
As of 1996
As of 2023
As of 2023
C166 EVs potentiate miR cardiac reprogramming via miR-148a-3p[9]
Cardiac regeneration through cellular reprogramming of fibroblasts into cardiomyocytes[11]
Cell-cycle regulation of sarcomere integrity-Role for Actn2 phosphorylation[9]
Engineering extracellular vesicles for targeted therapeutic delivery in the heart[9]
Hemoglobin inhibits fibroblast-to-cardiomyocyte reprogramming via TLR2/TLR4-dependent chromatin compaction[9]
Modifying miRs for effective reprogramming of fibroblasts to cardiomyocytes[9]
Novel approaches for cardiac reprogramming: Exosome delivery of reprogramming miRNAs and repressor targeting siRNAs[10]
2025 to 2029
Novel approaches for cardiac reprogramming using exosome delivery of reprogramming miRNAs and repressor targeting siRNAs[9]
2025 to 2029
Nucleosome repositioning in cardiac reprogramming[9]
Oversaw a study using cellular reprogramming to convert fibroblasts into cardiac muscle cells[12]
Precision Hypertension[9]
Skeletal muscle differentiation induces wide-ranging nucleosome repositioning in muscle gene promoters[9]
Sustained β-catenin activation via GSK3 inhibition promotes direct fibroblast-to-cardiomyocyte reprogramming[9]
The impact of aging on cardiac repair and regeneration[9]