Abstract
Heart failure (HF) is known as the final manifestation of cardiovascular diseases. Although cellular heterogeneity of the heart is well understood, the phenotypic transformation of cardiac cells in progress of HF remains obscure. This study aimed to analyze phenotypic transformation of cardiac cells in HF through human single-cell RNA transcriptome profile. Here, phenotypic transformation of cardiomyocytes (CMs), endothelial cells (ECs), and fibroblasts was identified by data analysis and animal experiments. Abnormal myosin subunits including the decrease in Myosin Heavy Chain 6, Myosin Light Chain 7 and the increase in Myosin Heavy Chain 7 were found in CMs. Two disease phenotypes of ECs named inflammatory ECs and muscularized ECs were identified. In addition, myofibroblast was increased in HF and highly associated with abnormal extracellular matrix. Our study proposed an integrated map of phenotypic transformation of cardiac cells and highlighted the intercellular communication in HF. This detailed definition of cellular transformation will facilitate cell-based mapping of novel interventional targets for the treatment of HF.
Highlights
Heart failure (HF) is a complex disease, which represents the final stage for several heart diseases, such as coronary heart disease and various cardiomyopathies
Single-cell sequencing data were collected from the GEO database which was composed of 10 human cardiac tissue samples, including HF caused by coronary heart disease, dilated cardiomyopathy, and normal tissues
Our study uncovered a host of previously unrecognized functions in endothelial cells (ECs) and FBs, for example, normal fibroblasts (Nor-FBs) can transform into Myo-FBs, accompanied by decreased collagen secretion and increased expression of muscle proteins
Summary
Heart failure (HF) is a complex disease, which represents the final stage for several heart diseases, such as coronary heart disease and various cardiomyopathies. ScRNA-seq was applied to distinguish the T cell type in the heart with myocardial infarction or myocardial ischemia/reperfusion injury and a phenotypically and functionally unique population of heart-regulated T cells was identified, which exert heart protective effects in many diseases [4]. These studies revealed the great potential of scRNA-seq in exploring the mechanism of heart failure, which will make cell therapy or cell transplantation a promising approach for restoring cardiac
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