Coming to the rescue, though, is Bcl-2-associated athanogene 3 (BAG3), a protein showed in a new study to help limit reperfusion injury. Enhancing the expression of BAG3 could prevent all of these bad things from happening, according to a new study from scientists at Temple University. New findings suggest that BAG3 could be the center of new therapeutics for reperfusion in heart attack patients.
BAG3 expression is beneficial by inactivating cell death pathways and activating autophagy, essentially reversing the negative influence of the toxic oxidizing substances produced after damage is done to the heart muscle. Scientists saw this effect in cultured cardiomyocytes during their study.
"After finding that a mutation in BAG3 caused heart failure in a Philadelphia family, we have been trying to figure out what the protein does in the heart," said senior investigator Dr. Arthur M. Feldman, MD, PhD, on how his team got to the results they found in the present study. "Now that we have a better understanding of its role and what happens when its levels are increased, we can investigate the possibility of targeting BAG3 in human patients using gene therapy or a small molecule."
Feldman’s study was recently published in the journal JCI Insight.
Source: Temple University Health System