Dichotomy between the transcriptomic landscape of naturally versus accelerated aged murine hearts.
Federica De MajoJana-Charlotte HegenbarthFrank RühleChristian BärThomas ThumMartine de BoerDirk Jan DunckerBlanche SchroenAnne-Sophie ArmandMonika StollLeon J De WindtPublished in: Scientific reports (2020)
We investigated the transcriptomic landscape of the murine myocardium along the course of natural aging and in three distinct mouse models of premature aging with established aging-related cardiac dysfunction. Genome-wide total RNA-seq was performed and the expression patterns of protein-coding genes and non-coding RNAs were compared between hearts from naturally aging mice, mice with cardiac-specific deficiency of a component of the DNA repair machinery, mice with reduced mitochondrial antioxidant capacity and mice with reduced telomere length. Our results demonstrate that no dramatic changes are evident in the transcriptomes of naturally senescent murine hearts until two years of age, in contrast to the transcriptome of accelerated aged mice. Additionally, these mice displayed model-specific alterations of the expression levels of protein-coding and non-coding genes with hardly any overlap with age-related signatures. Our data demonstrate very limited similarities between the transcriptomes of all our murine aging models and question their reliability to study human cardiovascular senescence.
Keyphrases
- single cell
- rna seq
- genome wide
- high fat diet induced
- dna repair
- dna methylation
- oxidative stress
- poor prognosis
- endothelial cells
- dna damage
- gene expression
- binding protein
- left ventricular
- wild type
- magnetic resonance
- mouse model
- heart failure
- copy number
- protein protein
- deep learning
- contrast enhanced
- atomic force microscopy
- single molecule
- high speed