As a healthy heart ages, it becomes more susceptible to cardiovascular diseases.
Though researchers have discovered that relaxin, an insulin-like hormone, suppresses atrial fibrillation (AF), inflammation, and fibrosis, the underlying mechanisms of these benefits are still unknown.
In a new study, researchers found how relaxin interacts with the body’s signaling processes to produce a fundamental mechanism that may improve heart disease treatment.
The research was conducted by a team at the University of Pittsburgh.
As the U.S. population ages, the rates of these age-associated diseases are expected to rise, requiring better treatment for this leading cause of death.
According to a report from the American Heart Association, the total direct medical costs of cardiovascular disease are projected to increase to $749 billion in 2035.
Relaxin is a reproductive hormone discovered in the early 20th century that has been shown to suppress heart disease symptoms
In this study, the team found that relaxin treatment reverses electrical remodeling in animal models by activating canonical Wnt signaling—a discovery that reveals a fundamental underlying mechanism behind relaxin’s benefits.
A better understanding of how relaxin interacts with the body may improve its efficacy as a therapy to treat heart disease in humans.
A common problem in age-associated heart disease is altered electrical signaling required for proper heart contraction.
When ions in the heart and their associated channels to enter or exit the heart are disrupted, complications occur.
Natural, healthy aging has been shown to be accompanied by changes in structure and function.
The reversal of some aspects of the aging process by relaxin is mediated by the reactivation of Wnt canonical signaling which may partly explain mechanisms of the aging process.
The team found increased prominent sodium channel, Nav1.5, in cells of the heart tissue may lead to better electrical signaling in the heart and may reduce susceptibility to cardiac rhythm disorders.
While these data provide new insight into relaxin’s mechanisms of action, further work is needed to understand the precise steps required for relaxin to alter Wnt signaling.
The lead author of the study is graduate student Brian Martin.
The study is published in Scientific Reports.
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