Why the study?
Heart failure represents a major cause of morbidity and mortality worldwide, but the specific cellular composition and associated gene expression of the healthy and failing human heart remained to be comprehensively defined.
Single cell transcriptomics reveals distinct cell-type specific transcriptional shifts and diversification in human heart failure, providing a resource for future investigation.
Transcriptomic maps of healthy and failing hearts remain hypothesis-generating; clinical translation requires prospective validation.
Heart failure represents a major cause of morbidity and mortality worldwide. Single cell transcriptomics have revolutionized our understanding of cell composition and associated gene expression across human tissues. Through integrated analysis of single cell and single nucleus RNA sequencing data generated from 45 individuals, we define the cell composition of the healthy and failing human heart. We identify cell specific transcriptional signatures of heart failure and reveal the emergence of disease associated cell states. Intriguingly, cardiomyocytes converge towards a common disease associated cell state, while fibroblasts and myeloid cells undergo dramatic diversification. Endothelial cells and pericytes display global transcriptional shifts without changes in cell complexity. Collectively, our findings provide a comprehensive analysis of the cellular and transcriptomic landscape of human heart failure, identify cell type specific transcriptional programs and states associated with disease, and establish a valuable resource for the investigation of human heart failure.
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Koenig et al. (2021) studied this question.
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