Gene expression profiling of the aging mouse cardiac myocytes
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Updated: Sep 29, 2026
Single Cell Transcriptional Profiling of Adult Mouse Cardiomyocytes
Published on: December 28, 2011
Natalya Bodyak1, Peter M Kang, Makoto Hiromura
1Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Insights
Cardiac aging leads to heart dysfunction due to altered gene expression in heart muscle cells. This study identifies key genes involved in aging hearts, offering insights into heart disease mechanisms.
Area of Science:
- Cardiology
- Molecular Biology
- Gerontology
Background:
- Heart disease is a leading cause of death, particularly in older adults.
- The molecular basis of age-related cardiac dysfunction is not well understood.
- Cardiac muscle cell (cardiomyocyte) aging involves structural and functional changes.
Purpose of the Study:
- To analyze gene expression changes in aging mouse heart muscle cells.
- To identify specific genes associated with cardiac aging.
- To understand the molecular mechanisms of age-related heart decline.
Main Methods:
- Comparison of complementary DNA (cDNA) libraries from young and aged mouse ventricular cardiomyocytes.
- Analysis of messenger RNA (mRNA) levels to identify age-related gene expression changes.
Main Results:
- Identified genes with altered mRNA levels in aged hearts.
- Observed decreased cellular adaptation and stress protection in aged hearts.
- Detected reduced mitochondrial electron transport system activity and cardiac-specific transcription factors.
- Noted similarities between cardiomyocyte aging gene expression profiles and those in heart disorders.
Conclusions:
- Cardiac aging involves significant changes in gene expression.
- These changes contribute to contractile dysfunction and reduced cellular resilience.
- Understanding these molecular alterations is crucial for addressing age-related heart disease.
Abstract:
Heart disease remains the most frequent cause of death in the general population with increasing incidence in the elderly population. The pathologic failure of the aging heart may be related to structural and functional alterations in cardiac muscle cells. However, the molecular mechanisms underlying the aging-related decline in cardiac muscle function are largely unknown. To provide the first analysis of cardiac aging at the level of gene expression, we established and compared cDNA libraries from apparently healthy young and aged mouse ventricular cardiac muscle cells. We report the identification of genes that exhibit aging-related changes of mRNA levels. Aging expression profiles in aged hearts indicate decreased cellular adaptation and protection against stress-induced injury together with the development of contractile dysfunction. The data suggest reduced activity of the mitochondrial electron transport system and reduced levels of cardiac-specific transcription regulators. The cardiomyocyte aging profile of gene expression displays similarities with known heart disorders. Genes whose mRNA levels change with aging in cardiomyocytes might profoundly affect pathological changes in the heart.
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