Researchers from the University of Utah (U of U) released a study last week detailing the importance of a key protein in heart cells, VDAC2, in potentially preventing heart failure. The study shows drug and therapeutic treatments that improve the signaling pathway for this protein can alleviate and reverse the effects of heart failure.
Stay one step ahead. Join our email list for the latest news.Subscribe
According to the study, the disruption in the signaling pathway of VDAC2 makes it harder for blood to pump through the body. The protein helps direct calcium to contract the heart in between beats, making it vital to keep the heart beating. The specific role in VDAC2 intracellular calcium dynamics and cardiac function is not well understood.
Stravros Drakos, MD, PhD, professor of medicine and director of cardiovascular research for the Division of Cardiology and U of U Health and senior author of the study, said:
“Based on our human and laboratory research, it appears that if VDAC2 is not working properly, then everything in the heart can cascade downward from there. If we can figure out ways to help this protein do its job again, then it’s possible that we might be able to address heart failure far earlier in the disease process.”
The study said this protein lies on the outer membrane of the mitochondria in heart cells and allows calcium to flow into the mitochondria. Mitochondria relies on calcium to create biochemical energy to keep cells alive, which places great importance on VDAC2 in monitoring calcium levels.
When VDAC2 is unable to communicate with the mitochondria and other cells around it, it makes the ebb and flow of calcium difficult for the mitochondria, which permeates throughout the heart. Tripura Sundari Shankar, lead author of the study and a graduate PhD student in Drakos lab, said:
“Our study shows the importance of VDAC2 in normal cardiac function. Through this unique role, VDAC2 emerges as a potential therapeutic target for heart failure patients.”
When VDAC2 was disabled in lab mice, calcium flow was severely impaired to the mitochondria leading to the improper beating of the heart. This led to an enlargement of the heart’s pumping chamber, the left ventricle, which made it harder for the heart to pump blood.
The study found restoring the protein’s functionality in the mice reversed the many effects leading to heart failure and prevented death.
This study appears in Nature Communications.