Cellular Phenotypic Transformation in Heart Failure Caused by Coronary Heart Disease and Dilated Cardiomyopathy: Delineating at Single-Cell Level
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Published on: March 22, 2017
Luojiang Zhu1, Wen Wang2, Changzhen Ren2
1Neurovascular Center, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai 200433, China.
Insights
This study reveals how heart cells, including cardiomyocytes, endothelial cells, and fibroblasts, change during heart failure (HF). Understanding these cellular transformations offers new targets for HF treatments.
Area of Science:
- Cardiovascular Biology
- Cellular and Molecular Medicine
- Genomics and Transcriptomics
Background:
- Heart failure (HF) represents the advanced stage of cardiovascular diseases.
- While cardiac cellular heterogeneity is known, the specific phenotypic changes in cardiac cells during HF progression are not fully understood.
Purpose of the Study:
- To investigate the phenotypic transformation of cardiac cells in heart failure using human single-cell RNA transcriptome profiles.
- To identify specific cellular changes in cardiomyocytes, endothelial cells, and fibroblasts during HF.
Main Methods:
- Analysis of human single-cell RNA transcriptome data.
- In vivo validation through animal experiments.
- Identification of molecular markers associated with cellular phenotypes.
Main Results:
- Cardiomyocytes (CMs) showed altered myosin subunit expression (decreased MYH6, MYL7; increased MYH7).
- Endothelial cells (ECs) exhibited two disease phenotypes: inflammatory and muscularized ECs.
- An increase in myofibroblasts, linked to abnormal extracellular matrix, was observed in HF.
Conclusions:
- An integrated map of cardiac cellular phenotypic transformation in HF was proposed.
- Intercellular communication pathways in HF were highlighted.
- Detailed cellular transformation data can guide the development of cell-based therapeutic targets for HF.
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.
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