Resources

Amrute, Lai et al. performed single-nucleus RNA sequencing and compared the cellular and transcriptomic features of hearts from non-diseased donors, from patients with heart failure who recovered systolic function after left ventricular assist device implantation and from patients who did not recover. The analyses identified cell-type-specific signatures of recovery and revealed the downregulation of RUNX1 expression in macrophages and fibroblasts as a predictor of recovery, as confirmed by in silico simulations and re-analysis of data from a mouse model of cardiac functional recovery.

Berg Luecke et al. developed an analytical platform, CellSurfer, that enables the quantitative profiling of cell surface proteome (surfaceome) from small samples, and they apply it to primary human heart cells. The analyses revealed LSMEM2 as a surface protein specific for healthy cardiomyocytes; important surfaceome differences between primary human cardiac cells and the pluripotent stem cell derivatives; and differences in the abundance of surface proteins between human failing and non-failing cardiomyocytes.

Deviatiiarov, Gams et al. provide an atlas of the actively transcribed regulatory elements (promoters and enhancers) in the human heart by performing cap analysis of gene expression (CAGE) on 21 healthy donor hearts and ten failing hearts from ischemic and non-ischemic cardiomyopathy. The data show how the alternative use of regulatory elements modulates the differential gene expression across different heart chambers, disease states and disease types.

Knight-Schrijver et al. use single-cell and single-nuclei RNA sequencing to profile the human fetal and adult epicardium in homeostatic conditions. The analysis shows fetal-specific epicardial gene programs that could support heart regeneration.

Mantri et al. used spatial transcriptomics and scRNA-seq combined with smFISH to characterize the pathogenesis of reovirus-induced myocarditis in neonatal mice. They report a key role for endothelial cells in modulating the inflammatory response to the virus and a role for cytotoxic T-cell-induced pyroptosis in the cardiac pathology.

Caudal, Tang, et al. use isobaric quantitative protein interaction reporter (iqPIR) technology to compare the mitochondrial protein interactome in healthy and failing murine hearts, providing molecular-level insights into complex mitochondrial remodeling in heart failure.

Koenig et al. present integrated single-cell and single-nucleus RNA-sequencing data of cardiac samples obtained from 27 healthy donors and 18 individuals with dilated cardiomyopathy. This extensive resource provides insights on cell composition and gene expression changes driven by the disease status, sex or age of the patients.

Using large-scale single-nucleus transcriptomics, Nicin et al. report insights into human cardiac hypertrophy, caused by pressure overload, at single-cell resolution. The authors show that intercellular communication, particularly via the Eph receptor tyrosine kinase EPHB1, is impaired in human cardiomyopathy.