James E. Hudson

This study shows that gene therapy with AAV-ALPK3 improves heart function in mouse and human models of cardiomyopathy caused by ALPK3 variants.

This study compares sixteen iPSC-CM differentiation protocols to identify how protocol-dependent cell states affect disease modeling capacity for cardiovascular conditions.

This study identifies prenylation as a regulator of cardiomyocyte proliferation through multiple targets, suggesting its potential for cardiac regeneration.

This study identifies glycophagy dysregulation as a mechanism of diabetic heart disease and shows that Gabarapl1 gene therapy improves cardiac function in diabetic mice and human cardiac organoids.

The paper shows that inhibiting contractile function in cardiomyocytes reactivates the cell cycle, suggesting active contraction maintains differentiation and cell cycle arrest.

This study shows that maturing human cardiac organoids enhances disease modeling and drug discovery by mimicking in vivo development and enabling therapeutic testing for DSP cardiomyopathy.

The paper develops a resource to improve cardiac modelling protocols using hPSC-CMs by analyzing decades of research data and providing tools for protocol benchmarking.

This study shows that modified mRNA encoding Myc and Cyclin T1 can induce cardiomyocyte proliferation and improve cardiac function after myocardial injury in mice.

The paper identifies UFMylation as a negative regulator of skeletal muscle function through proteome-wide systems genetics in mice and validates it in a disease model.

This study identifies HOPX as a molecular switch regulating cardiomyocyte progenitor and maturation gene programs, linking it to cardiac function and genetic variation.

This study identifies Gabarapl1 as a regulator of glycophagy in diabetic cardiomyopathy, showing its role in preventing glycogen accumulation and diastolic dysfunction.

The paper maps cardiac differentiation at single-cell resolution, identifies HOPX dysregulation, and shows hypertrophic signaling is required for HOPX transcription in hPSC-derived cardiomyocytes.