Gene expression profiling of aged mouse cardiac myocytes revealed decreased cellular adaptation, reduced mitochondrial electron transport activity, and similarities with known heart disorders.
What are the gene expression changes underlying the aging-related decline in cardiac muscle function in mouse ventricular cardiomyocytes?
Gene expression profiling of aging mouse cardiomyocytes reveals reduced mitochondrial function and stress adaptation, providing molecular insights into age-related contractile dysfunction.
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.
Natalya D. Bodyak (Fri,) conducted a other in Cardiac aging. Aged mouse ventricular cardiac muscle cells vs. Young mouse ventricular cardiac muscle cells was evaluated on Aging-related changes of mRNA levels. Gene expression profiling of aged mouse cardiac myocytes revealed decreased cellular adaptation, reduced mitochondrial electron transport activity, and similarities with known heart disorders.