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Loss of dynamic regulation of G protein-coupled receptor kinase 2 by nitric oxide leads to cardiovascular dysfunction with aging

Melissa Lieu, Christopher J. Traynham, Claudio de Lucia, Jessica Pfleger, Michela Piedepalumbo, Rajika Roy, Jennifer Petovic, Gavin Landesberg, Steven J. Forrester, Matthew Hoffman, Laurel A. Grisanti, Ancai Yuan, Erhe Gao, Konstantinos Drosatos, Satoru Eguchi, Rosario Scalia, Douglas G. Tilley, Walter J. Koch

2020American Journal of Physiology-Heart and Circulatory Physiology15 citationsDOIOpen Access PDF

Abstract

Research on G protein-coupled receptor kinase 2 (GRK2) in the setting of cardiovascular aging is largely unknown despite its strong established functions in cardiovascular physiology and pathophysiology. This study uses a mouse model of chronic GRK2 overactivity to further investigate the consequences of long-term GRK2 on cardiac function and structure. We report for the first time that chronic GRK2 overactivity was able to cause cardiac dysfunction and remodeling independent of surgical intervention, highlighting the importance of GRK activity in aged-related heart disease.

Topics & Concepts

Beta adrenergic receptor kinaseNitric oxidePathophysiologyMedicineG protein-coupled receptor kinaseCardiac dysfunctionReceptorDiseaseCardiac function curveInternal medicineBioinformaticsProtein kinase ACardiologyKinaseHeart failureEndocrinologyBiologyG protein-coupled receptorCell biologyReceptor Mechanisms and SignalingNitric Oxide and Endothelin EffectsCardiac electrophysiology and arrhythmias
Loss of dynamic regulation of G protein-coupled receptor kinase 2 by nitric oxide leads to cardiovascular dysfunction with aging | Litcius