Heart failure & cardiomyopathies
Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling
Authors' conclusion
The present results of single-nucleus RNA sequencing and heart failure mouse model indicated that ATP5F1A could mediate CRR and supported the development of therapeutics for overexpressing ATP5F1A in promoting CRR.
Study context
- Population
- LV tissue of patients with left ventricular assist device (cardiac reverse remodeling (CRR), no CRR) and normal controls; HF mouse models126,156 nuclei
- Participants
- 4 / 4 / 4
- Comparison
- CRR vs no CRR vs normal controls; ATP5F1A overexpression in HF mouse models
- Normal controlsn = 4reference
- CRRn = 4
- No CRRn = 4
Methodological detailssingle-nucleus RNA sequencing, mouse models (TAC and dilated cardiomyopathy HF)
- Single-nucleus RNA sequencing
- Mouse models (TAC and dilated cardiomyopathy HF)
Main finding
As reported in the abstract
- 10 cell types identified among 126 156 nuclei
- Cardiomyocytes in CRR expressed higher ATP5F1A than the other 2 groups
- Macrophages in CRR expressed more anti-inflammatory genes and functioned in angiogenesis
- Endothelial cells elevated in no CRR involved in inflammatory response
- Cardiomyocyte-specific AAV9 ATP5F1A overexpression improved heart function and morphology (echocardiography)
- ATP5F1A overexpression reduced fibrosis and cardiomyocyte size in HF mice
Original publication
Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling. Circ Heart Fail. Published 24 June 2024. doi:10.
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