David A. Elliott

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

The paper identifies a compound that selectively promotes cardiomyocyte proliferation through specific cell cycle mechanisms without affecting other cell types.

This study identifies a homozygous SECISBP2 variant causing lethal perinatal cardiomyopathy through loss of selenoprotein function, including GPX4, and suggests a ferroptosis mechanism.

This study uses proteomics to identify a cryptic JPH2 loss-of-function in a paediatric DCM patient, revealing a novel mechanism of recessive disease.

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 evaluates the clinical validity of heterozygous ALPK3 loss-of-function variants as a cause of hypertrophic cardiomyopathy, finding strong gene-disease association with reduced penetrance.

This study benchmarks spatial transcriptomics methods by comparing 6 SVG identification tools across 14 datasets, revealing discrepancies in results.

VR-Omics automates integration of multi-slice spatial transcriptomics data in 2D and 3D, revealing dysregulated metabolic networks in paediatric cardiac rhabdomyomas.

This paper develops a 3D spatial transcriptomic atlas of the mouse heart and provides a web tool for analysis and visualization.

The paper identifies a conserved enhancer in the FLT1 locus that drives cardiovascular expression and modulates angiogenesis pathways in vitro and in vivo.

The paper identifies distinct homeostatic and growth adult stem cell populations in medaka gills, showing their spatial separation and functional specialization.