Characterization of cardiac effects of OPA1 protein promotion in transgenic animal model

Abstract Introduction Mitochondria forms a dynamic network in cells, which is regulated by the balance between mitochondrial fusion and fission. The inhibition of fission could result positive effects acute ischemic/reperfusion injury models, due to prevention membrane potential fall that goes along with processes. However, chronic models disadvantageous because it obstructs elimination damaged fragments. OPA1 – view previous results possible therapy target, as promoter structure stabilizer protein. Methods We used transgenic mice OMA1 YME1L cleavage spots were deleted. This resulted higher representation L-OPA1 compared S-OPA1. After genotyping model validation all animals examined echocardiograph ECG on two occasions, at week 11 36. Histology samples made from hearts, case morphology remodelling examination. Cardiomyocytes isolated neonatal determine efficiency respiration SeaHorse assay method. Results Capillary Western immunoassay proved presence concentration TG animals. Echocardiographic examination showed significant ejection fraction reduction 36, but histology not be observed. was decreased WT animals, according assay. Conclusion protein promotion has negative effect systolic function during ageing. confirmed volume overload ventricular remodeling did manifested. reason behind loss pump might least partly energy deficit respiratory failure damage quality control pathways. Funding Acknowledgement Type funding sources: Public grant(s) National budget only. Main source(s): research Hungary funded NKFIH within framework project TKP2021-EGA-17.