Researches Target acyl-CoA Level For Treating Heart Failures
Our hearts get the energy necessary to function well By burning fats and glucose. In the context of this statement, a compound has been identified by the Researchers at Ohio State University that plays a key role in fat metabolism but that reduces when the heart gets stressed. Restoring it could lower the risk of heart failure.
Doug Lewandowski a Ph.D. Researcher who focuses on cardiac metabolism from Ohio university stated that – Before any physical signs or symptoms of heart failure emerge, chronically stressed cardiac cells undergo changes to adapt, but the alterations do not necessarily make things better.
Lewandowski’s team members found that deficiencies of a reactive fat compound called acyl-CoA interrupt the heart’s energy production cycle which leads to toxic fat accumulation that impairs its ability to function and pump properly. The researchers also analyzed mouse models of heart failure, in addition to human heart tissue obtained from patients before and after left ventricular a
ssist device (LVAD) implantation. The acyl-CoA level is approx 60% lower in a heart with complexities compared to normal ones.An enzyme called acyl-CoA synthetase (ACSL1) catalyzes the uptake and activation of long-chain fatty acids that is a process which creates an acyl-CoA. The team analyzed mice that overexpress the ACSL1-encoding gene by exposing them to stress conditions. The mice created normal levels of acyl-CoA, fatty acid trafficking was enhanced, and heart failure risk was reduced or delayed, the team reported.
The hearts retained their ability to burn fat and generate energy by maintaining the fat compound acyl-CoA
The scientists observed that In human heart cells the levels of acyl-CoA returned to normal in post-LVAD samples which makes sense because whenever the failing heart has extra help from the pump device, it does not have to work as hard under stress.
Various new targets which might help tackle heart ailments have come to light lately. Imperial College London Researchers pinpointed a protein named MAP4K4, which sends stress signals during a cardiac arrest that eventually result in heart damage.
Researchers at the Scripps Research Institute found the GPR68 protein as a potential drug target that can help dilate blood vessels and keep the heart healthy.
Lewandowski stated that – He and his team members are planning to examine how increasing acyl-CoA levels results in heart protection and they hopeing to use advanced imaging to monitor fat metabolism in patients hearts targeting the normalization of acyl-CoA through gene or drug therapy or, possibly, dietary protocols which could open new possibilities to prevent or mitigate heart failure.
