Cellular Phenotypic Transformation in Heart Failure Caused by Coronary Heart Disease and Dilated Cardiomyopathy: Delineating at Single-Cell Level
Luojiang Zhu,
Wen Wang,
Changzhen Ren,
Yangkai Wang,
Guanghao Zhang,
Jianmin Liu,
Weizhong Wang
Affiliations
Luojiang Zhu
Neurovascular Center, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai 200433, China
Wen Wang
Department of Marine Biomedicine and Polar Medicine, Naval Medical Center, Naval Medical University (Second Military Medical University), Shanghai 200433, China
Changzhen Ren
Department of Marine Biomedicine and Polar Medicine, Naval Medical Center, Naval Medical University (Second Military Medical University), Shanghai 200433, China
Yangkai Wang
Department of Marine Biomedicine and Polar Medicine, Naval Medical Center, Naval Medical University (Second Military Medical University), Shanghai 200433, China
Guanghao Zhang
Neurovascular Center, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai 200433, China
Jianmin Liu
Neurovascular Center, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai 200433, China
Weizhong Wang
Department of Marine Biomedicine and Polar Medicine, Naval Medical Center, Naval Medical University (Second Military Medical University), Shanghai 200433, China
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.
