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Single Cell Transcriptional Profiling of Adult Mouse Cardiomyocytes
Published on: December 28, 2011
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A single-cell transcriptomic landscape of primate arterial aging.
Weiqi Zhang1,2,3,4,5, Shu Zhang6,7, Pengze Yan3,8
1CAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100101, China.
Nature Communications
|May 7, 2020
Summary
Aging impairs blood vessels, but mechanisms remain unclear. This study identifies FOXO3A as a key gene downregulated during aging, driving vascular dysfunction and offering new treatment targets for cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Aging Biology
- Genomics
Background:
- Vascular aging contributes to cardiovascular diseases, but cellular and molecular mechanisms are not fully understood.
- Primate models offer valuable insights into human aging processes.
Purpose of the Study:
- To investigate the single-cell transcriptomic changes in primate arteries during aging.
- To identify key molecular regulators of vascular aging.
Main Methods:
- Single-cell RNA sequencing of aortas and coronary arteries from young and old cynomolgus monkeys.
- Gene network analysis to identify transcriptional regulators.
- Functional validation using human vascular endothelial cells.
Main Results:
- Identified distinct molecular signatures for aortic and coronary vasculatures.
- Discovered that FOXO3A, a longevity-associated transcription factor, is downregulated in multiple vascular cell types during aging.
- Demonstrated that FOXO3A inactivation in human cells mimics age-related vascular defects.
Conclusions:
- FOXO3A downregulation is a critical driver of arterial endothelial aging.
- This study provides a comprehensive resource for understanding primate arterial aging.
- Findings suggest FOXO3A as a potential therapeutic target for age-associated vascular disorders.
