VDAC2 Targeted Therapeutics Could Possibly Reduce Chronic Heart Failure, According to University of Utah Health-led Study

VDAC2 Targeted Therapeutics Could Possibly Reduce Chronic Heart Failure According to University of Utah Health led Study

University of Utah Health researchers led an international study investigating whether a protein involved with regulating calcium signaling within heart cells could help prevent chronic heart failure. Disrupting the signaling pathway of VDAC2, the protein, triggers severe impairment of heart cell contraction, making it more difficult for the heart to deliver blood to the body. Could it be that therapeutic treatments targeting VDAC2 could help alleviate heart failure? Stavros Drakos, MD, senior author of the study, suggests that if this protein isn't working correctly, then "everything in the heart can cascade downward from there." The goal moving forward, according to the Utah-based investigator: Find a way to help VDAC2 do its job.


Senior University of Utah science writer Doug M. Dollemore recently authored a University of Utah press release showcasing the study, also recently published in Nature Communications. Dollemore articulated that it's no secret that calcium plays a pivotal role in the heart. For example, "Between heartbeats, calcium levels in heart muscle cells (myocytes) diminish, allowing the cell to relax. During contraction, a large amount of ca...

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