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New target for heart failure therapy identified
March 17, 2009(PHILADELPHIA) A novel signaling pathway plays a significant role in the production of aldosterone, a hormone that promotes heart failure after a myocardial infarction, according to a study conducted by Thomas Jefferson University researchers.
The findings, which will be published online this week in Proceedings of the National Academy of Sciences, show that aldosterone production is mediated by a protein called beta-arrestin-1. Beta-arrestin-1 binds to angiotensin II receptors when they are activated by angiotensin II.
Aldosterone is secreted by the adrenal cortex. Its levels are elevated in chronic heart failure, and its presence contributes to morbidity and mortality of the disease. It contributes to heart failure progression and diminished cardiac function after myocardial infarction.
The production of aldosterone was previously thought to be solely the result of the activation of G-proteins, which are also activated when angiotensin II binds to its receptors, according to Anastasios Lymperopoulos, Ph.D., a Post-Doctoral Research Fellow in the Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy at Jefferson Medical College of Thomas Jefferson University.
"The bottom line is that in order to effectively suppress aldosterone production, you need to inhibit beta-arrestin-1 in addition to inhibiting G-proteins," said Dr. Lymperopoulos, who is the lead author of the study.
All the drugs currently available for suppression of aldosterone by angiotensin II primarily target G-protein signaling pathways. However, Walter Koch, Ph.D., the W.W. Smith Professor of Medicine and the Director of the Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy, said that these data clearly show that beta-arrestin1 plays a more significant role in aldosterone secretion than G-proteins.
"Aldosterone secretion is dependent on beta-arrestin-1," Dr. Koch said. "It may not be independent of G-proteins, but beta-arrestin-1 is definitely the critical player. The goal should be to find a new antagonist that can block beta-arrestin-1 and G-protein activation equally well. Doing so would lead to lower aldosterone levels at its source and alleviate negative remodeling processes in the injured heart."
Thomas Jefferson University
The production of aldosterone was previously thought to be solely the result of the activation of G-proteins, which are also activated when angiotensin II binds to its receptors, according to Anastasios Lymperopoulos, Ph.D., a Post-Doctoral Research Fellow in the Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy at Jefferson Medical College of Thomas Jefferson University.
"The bottom line is that in order to effectively suppress aldosterone production, you need to inhibit beta-arrestin-1 in addition to inhibiting G-proteins," said Dr. Lymperopoulos, who is the lead author of the study.
All the drugs currently available for suppression of aldosterone by angiotensin II primarily target G-protein signaling pathways. However, Walter Koch, Ph.D., the W.W. Smith Professor of Medicine and the Director of the Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy, said that these data clearly show that beta-arrestin1 plays a more significant role in aldosterone secretion than G-proteins.
"Aldosterone secretion is dependent on beta-arrestin-1," Dr. Koch said. "It may not be independent of G-proteins, but beta-arrestin-1 is definitely the critical player. The goal should be to find a new antagonist that can block beta-arrestin-1 and G-protein activation equally well. Doing so would lead to lower aldosterone levels at its source and alleviate negative remodeling processes in the injured heart."
Thomas Jefferson University
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Young athletes need dual screening tests for heart defects, study suggests
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Protein changes in heart strengthen link between Alzheimer's disease and chronic heart failure
A team of U.S., Canadian and Italian scientists led by researchers at Johns Hopkins report evidence from studies in animals and humans supporting a link between Alzheimer's disease and chronic heart failure, two of the 10 leading causes of death in the United States.
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Many heart attack patients have high levels of cardiac biomarkers in the blood for several months after leaving the hospital, with more shortness of breath and chest pain, according to a Henry Ford Hospital study.
Tiny particles can deliver antioxidant enzyme to injured heart cells
Researchers at Emory University and the Georgia Institute of Technology have developed microscopic polymer beads that can deliver an antioxidant enzyme made naturally by the body into the heart.
New study links vitamin D deficiency to cardiovascular disease and death
While mothers have known that feeding their kids milk builds strong bones, a new study by researchers at the Heart Institute at Intermountain Medical Center in Salt Lake City suggests that Vitamin D contributes to a strong and healthy heart as well - and that inadequate levels of the vitamin may significantly increase a person's risk of stroke, heart disease, and death, even among people who've never had heart disease.
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