RSK3: A regulator of pathological cardiac remodeling

Eliana C. Martinez, Catherine L. Passariello, Jinliang Li, Christopher J. Matheson, Kimberly Dodge-Kafka, Philip Reigan, Michael S. Kapiloff

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)331-337
Number of pages7
JournalIUBMB life
Issue number5
StatePublished - May 1 2015


  • heart
  • hypertrophy
  • mAKAP
  • remodeling
  • ribosomal S6 kinase
  • scaffold
  • signal transduction

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics
  • Clinical Biochemistry
  • Cell Biology


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