title: RSK3: A regulator of pathological cardiac remodeling.
abstract: The family of p90 ribosomal S6 kinases (RSKs) are pleiotropic effectors for extracellular signal-regulated kinase signaling pathways. Recently, RSK3 was shown to be important for pathological remodeling of the heart. Although cardiac myocyte hypertrophy can be compensatory for increased wall stress, in chronic heart diseases, this nonmitotic cell growth is usually associated with interstitial fibrosis, increased cell death, and decreased cardiac function. Although RSK3 is less abundant in the cardiac myocyte than other RSK family members, RSK3 appears to serve a unique role in cardiac myocyte stress responses. A potential mechanism conferring the unique function of RSK3 in the heart is anchoring by the scaffold protein muscle A-kinase anchoring protein β (mAKAPβ). Recent findings suggest that RSK3 should be considered as a therapeutic target for the prevention of heart failure, a clinical syndrome of major public health significance.
authors.affiliation: Cardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, Division of Cardiology, Department of Pediatrics, Miller School of Medicine, University of Miami, Miami, FL, USA.
authors.forename: Eliana C
authors.initials: EC
authors.lastname: Martinez
authors.affiliation: Cardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, Division of Cardiology, Department of Pediatrics, Miller School of Medicine, University of Miami, Miami, FL, USA.
authors.forename: Catherine L
authors.initials: CL
authors.lastname: Passariello
authors.affiliation: Cardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, Division of Cardiology, Department of Pediatrics, Miller School of Medicine, University of Miami, Miami, FL, USA.
authors.forename: Jinliang
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado, Aurora, CO, USA.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Matheson
authors.affiliation: Calhoun Center for Cardiology, University of Connecticut Health Center, Farmington, CT, USA.
authors.forename: Kimberly
authors.initials: K
authors.lastname: Dodge-Kafka
authors.affiliation: Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado, Aurora, CO, USA.
authors.forename: Philip
authors.initials: P
authors.lastname: Reigan
authors.affiliation: Cardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, Division of Cardiology, Department of Pediatrics, Miller School of Medicine, University of Miami, Miami, FL, USA.
authors.forename: Michael S
authors.initials: MS
authors.lastname: Kapiloff
mesh_terms: D000818:Animals; D006801:Humans; D032383:Myocytes, Cardiac / Q000473:pathology*; D038744:Ribosomal Protein S6 Kinases, 90-kDa / Q000378:metabolism; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000502:physiology*; D013312:Stress, Physiological
chemical_list: C496901:Kcnn3 protein, rat; D051640:Small-Conductance Calcium-Activated Potassium Channels; D038744:Ribosomal Protein S6 Kinases, 90-kDa
keywords: Keywords ribosomal S6 kinase; heart; hypertrophy; mAKAP; remodeling; scaffold; signal transduction