AnalyzeDirect

A myocardial infarction, commonly referred to as a heart attack, is caused by sudden restriction of circulating blood to the heart due to blockage of a coronary artery. As prolonged ischemia (lack of blood) and hypoxia (diminished oxygen levels) may lead to irreversible damage of myocardial tissue, finding new ways to limit their negative consequences is a challenging task.

Adverse ventricular remodeling and myocardial injury are two of them most severe outcomes of heart attacks. As several studies have shown that Transient Receptor Potential Vanilloid 4 (TRPV4) is a crucial protein involved in both mechanisms, researchers from St. Joseph’s Hospital and Medical Center, Phoenix, hypothesized that deletion of the TRPV4 gene would benefit recovery after myocardial injury.

To further scrutinize this hypothesis, the investigators compared the effects of myocardial infarction induced by permanent coronary artery ligation in mice without the gene that codifies for this protein and in controls. One week after the surgical procedure, cardiac functional parameters such as ventricular end diastolic volume, ventricular end systolic volume, ventricular ejection fraction and ventricular mass index were measured from MRIs using Analyze software.

The information collected from the scans indicated that mice that did not express the protein maintained close to normal values and showed higher survival trends than wild type ones. In fact, TRPV4 is thought to be the major promoter of fibroblast differentiation into myofibroblasts, cells that are abundant in infarct tissue and play an important role in adverse cardiac remodeling. Therefore, TRPV4 inhibition, which resulted in reduced levels of myofibroblasts, proved to be pivotal for improved cardiac function.

This study provides valuable information on how to preserve myocardial activity and structure in response to a heart attack. TRPV4 inhibition prior to an ischemic event may, therefore, be considered a potential therapeutic strategy able to reduce the negative effects of myocardial infarction.

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