Decreasing TRAF3IP2 protein may treat ischemic heart disease
New study shows that the TRAF3 Interacting Protein 2 (TRAF3IP2) could be a potential therapeutic target in ischemic heart disease.
The study, “Targeting TRAF3IP2 by Genetic and Interventional Approaches Inhibits Ischemia/Reperfusion-induced Myocardial Injury and Adverse Remodeling”, was reported January 4, 2017 in the Journal of Biological Chemistry.
Heart attack is the number one cause of death in the USA. The Centers for Disease Control and Prevention (CDC) estimates that someone in the USA has a heart attack every 43 seconds. Moreover, approximately 1 in 6 people who experience a heart attack die as a result.
A heart attack occurs when blood flow to the heart is blocked. This causes damage to your heart muscle. To reduce heart muscle damage, it is crucial to re-establish blood supply. Opening a blocked coronary artery can be a way to re-establish blood supply and thus prevent sudden death, but it can lead to oxidative stress and inflammation in the heart, which may eventually result in heart failure. So far, no solution is available to settle this problem.
The protein TRAF3IP2 is an oxidative stress-responsive cytoplasmic adapter molecule, and an important mediator of autoimmune and inflammatory responses. The team previously found that TRAF3IP2 plays a role in initiating cardiovascular inflammatory responses. For the new study, the team uncovered that decreasing the amount of TRAF3IP2 can minimize inflammation that results from opening the blockage.
The researchers used ultrasound technology to deliver a TRAF3IP2 inhibitor (phosphorothioated TRAF3IP2 antisense oligonucleotides) to the heart of mice. Once inside the heart, the inhibitor was released to target the TRAF3IP2 protein. After having an arterial blockage opened, the treated mice had a significant reduction in heart damage. The results showed that targeting TRAF3IP2 could be a way to alleviate post-heart attack injury.
The study was conducted by researchers from University of Texas Health Science Center, University of Missouri School of Medicine, Harry S. Truman Memorial Veterans Hospital, Dalton Cardiovascular Research Center, and National Institutes of Health.
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