Cellular Phenotypic Transformation in Heart Failure Caused by Coronary Heart Disease and Dilated Cardiomyopathy: Delineating at Single-Cell Level.
Luojiang ZhuWen WangChangzhen RenYangkai WangGuanghao ZhangJianmin LiuWei-Zhong WangPublished in: Biomedicines (2022)
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.
Keyphrases
- single cell
- heart failure
- induced apoptosis
- acute heart failure
- endothelial cells
- extracellular matrix
- rna seq
- left ventricular
- cell cycle arrest
- data analysis
- binding protein
- oxidative stress
- cardiovascular disease
- high throughput
- gene expression
- stem cells
- cell death
- type diabetes
- dna methylation
- endoplasmic reticulum stress
- cell therapy
- signaling pathway
- mesenchymal stem cells
- metabolic syndrome
- cardiac resynchronization therapy
- cardiovascular events
- pi k akt
- cardiovascular risk factors