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Targeting the Adrenal Gland Could Be Key Against Heart Failure

pled receptor kinase 2, essentially turning them off. Using gene therapy to block adrenal gland GRK2 in animals in heart failure, the scientists were able to get the alpha 2 receptors working again and also found that the beta adrenergic receptors on the heart worked better as well.

“We’ve shown that in the adrenal gland, resetting the alpha adrenergic receptors by inhibiting GRK2 causes more normal regulation and the proper feedback control, and catecholamines are lowered,” explains Dr. Koch, who also heads the George Zallie and Family Laboratory of Cardiovascular Gene Therapy in the Department of Medicine. “If less catecholamine is presented to the heart, then the beta receptors restabilize and that improves heart function. The heart is allowed to relax and get better.”

“This is the first time anyone has identified a molecular mechanism involved in such sympathetic overdrive in heart failure,” adds study first author Anastasios Lymperopoulos, Ph.D., a postdoctoral fellow in the Center for Translational Medicine, and means that adrenal gland GRK2 becomes a new target for heart failure medications.

“GRK2 inhibitors would be a totally new class of drugs if they come on the market,” Dr. Koch says, adding that eventually, human gene therapy for heart failure could be feasible.
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