David John

This study shows that loss of KDM6A in hematopoietic cells impairs cardiac recovery after heart failure by causing epigenetic changes in myeloid cells that increase inflammation and worsen cardiac outcomes.

This paper uses single-nucleus RNA sequencing to analyze HFpEF myocardium, identifying transcriptional changes in cardiomyocytes, endothelial cells, fibroblasts, and macrophages that suggest metabolic, inflammatory, and fibrotic mechanisms.

This study identifies differentially explained genes in heart failure subtypes using neural networks and XAI tools to improve understanding of molecular mechanisms.

This study identifies vascular niches as key hotspots for age-related inflammation and fibrosis in cardiac tissue using single-nucleus RNA sequencing and spatial transcriptomics.

This study identifies ZBTB16 as a critical regulator of endothelial function in aging, showing its protective role against cardiac dysfunction through suppression of pro-fibrotic signaling.

The paper identifies reduced STAT3 expression in cardiac pericytes in HFpEF and shows its loss leads to senescence and impaired adhesion.

This study identifies decorin as a factor induced by aging that contributes to cardiac inflammation and diastolic dysfunction through pro-inflammatory effects in the myocardium.

This study shows that loss of RGS5 in pericytes with age leads to cardiac dysfunction and fibrosis by altering pericyte function and activating fibroblasts.

This study identifies circPLOD2 as a hypoxia-regulated circRNA that modulates pericyte function by regulating KLF4, affecting proliferation and vascular interactions.

The paper introduces a cross-species integration pipeline for scRNA-seq data, validated on heart failure datasets from mice and humans, improving ortholog assignment and enabling pathway comparison.

This study compares common scRNA-seq alignment tools, finding differences in runtime, cell and gene detection, and potential artifacts, highlighting the impact of mapping strategies on analysis outcomes.