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RSK3: A regulator of pathological cardiac remodeling

Eliana C Martinez1, Catherine L Passariello1, Jinliang Li1

  • 1Cardiac 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.

IUBMB Life
|May 20, 2015
PubMed

Insights

p90 ribosomal S6 kinase 3 (RSK3) plays a unique role in cardiac stress responses and pathological heart remodeling. Targeting RSK3 may prevent heart failure, a significant public health issue.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Signal Transduction

Background:

  • p90 ribosomal S6 kinases (RSKs) are key effectors in extracellular signal-regulated kinase (ERK) signaling.
  • RSK3 has emerged as a critical factor in pathological cardiac remodeling, contributing to heart disease progression.
  • Cardiac myocyte hypertrophy, while initially compensatory, can lead to fibrosis, cell death, and impaired function in chronic heart conditions.

Purpose of the Study:

  • To elucidate the unique role of RSK3 in cardiac myocyte stress responses.
  • To investigate the potential of RSK3 as a therapeutic target for preventing heart failure.

Main Methods:

  • The study focuses on the functional significance of RSK3 within cardiac myocytes.
  • Investigates the interaction of RSK3 with the scaffold protein muscle A-kinase anchoring protein β (mAKAPβ).

Main Results:

  • RSK3, despite lower abundance, exhibits a distinct function in cardiac myocyte stress.
  • Anchoring by mAKAPβ may confer RSK3's unique role in the heart.
  • RSK3 is implicated in the pathological remodeling associated with heart failure.

Conclusions:

  • RSK3 is a critical mediator of cardiac stress responses and pathological remodeling.
  • Targeting RSK3 presents a promising therapeutic strategy for the prevention of heart failure.
  • Understanding RSK3's interaction with mAKAPβ is key to its therapeutic potential.

Keywords:
Keywords ribosomal S6 kinasehearthypertrophymAKAPremodelingscaffoldsignal transduction

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