E-MTAB-11268
The atlas of the human hypertrophied heart reveals impaired cell communication
Pathological cardiac hypertrophy is a leading cause of heart failure. The understanding of disease mechanisms is primarily based on experimental models, but knowledge of the full repertoire of cardiac cells and their gene expression profiles in the human heart is missing. Here, using large-scale single-nucleus transcriptomes, we highlight the transcriptional response of cardiomyocytes to pressure overload in humans with stenosis of the aortic valve and disclose major alterations in cellular cross-talk. Cardiomyocytes showed a reduction of incoming connections with endothelial cells and fibroblasts. Particularly Eph receptor tyrosine kinases, including the predominant EPHB1 gene, were significantly down-regulated in cardiomyocytes of the hypertrophied heart. We compared 5 AS patients to healthy patients from the human heart cell ATLAS (https://www.heartcellatlas.org). This repository contains the raw files from the single nuclei RNA-SEQ.
Pathological cardiac hypertrophy is a leading cause of heart failure. The understanding of disease mechanisms is primarily based on experimental models, but knowledge of the full repertoire of cardiac cells and their gene expression profiles in the human heart is missing. Here, using large-scale single-nucleus transcriptomes, we highlight the transcriptional response of cardiomyocytes to pressure overload in humans with stenosis of the aortic valve and disclose major alterations in cellular cross-talk. Cardiomyocytes showed a reduction of incoming connections with endothelial cells and fibroblasts. Particularly Eph receptor tyrosine kinases, including the predominant EPHB1 gene, were significantly down-regulated in cardiomyocytes of the hypertrophied heart. We compared 5 AS patients to healthy patients from the human heart cell ATLAS (https://www.heartcellatlas.org). This repository contains the raw files from the single nuclei RNA-SEQ.