RSK3

A regulator of pathological cardiac remodeling

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

Research output: Contribution to journalArticle

6 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)331-337
Number of pages7
JournalIUBMB Life
Volume67
Issue number5
DOIs
StatePublished - May 1 2015

Fingerprint

Cardiac Myocytes
90-kDa Ribosomal Protein S6 Kinases
Ribosomal Protein S6 Kinases
Muscle Proteins
Extracellular Signal-Regulated MAP Kinases
Cardiomegaly
Protein Kinases
Heart Diseases
Cell growth
Fibrosis
Public health
Chronic Disease
Cell Death
Cell death
Heart Failure
Public Health
Scaffolds
Phosphotransferases
Growth
Proteins

Keywords

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

ASJC Scopus subject areas

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

Cite this

Martinez Valencia, E. C., Passariello, C. L., Li, J., Matheson, C. J., Dodge-Kafka, K., Reigan, P., & Kapiloff, M. S. (2015). RSK3: A regulator of pathological cardiac remodeling. IUBMB Life, 67(5), 331-337. https://doi.org/10.1002/iub.1383

RSK3 : A regulator of pathological cardiac remodeling. / Martinez Valencia, Eliana Cecilia; Passariello, Catherine L.; Li, Jinliang; Matheson, Christopher J.; Dodge-Kafka, Kimberly; Reigan, Philip; Kapiloff, Michael S.

In: IUBMB Life, Vol. 67, No. 5, 01.05.2015, p. 331-337.

Research output: Contribution to journalArticle

Martinez Valencia, EC, Passariello, CL, Li, J, Matheson, CJ, Dodge-Kafka, K, Reigan, P & Kapiloff, MS 2015, 'RSK3: A regulator of pathological cardiac remodeling', IUBMB Life, vol. 67, no. 5, pp. 331-337. https://doi.org/10.1002/iub.1383
Martinez Valencia EC, Passariello CL, Li J, Matheson CJ, Dodge-Kafka K, Reigan P et al. RSK3: A regulator of pathological cardiac remodeling. IUBMB Life. 2015 May 1;67(5):331-337. https://doi.org/10.1002/iub.1383
Martinez Valencia, Eliana Cecilia ; Passariello, Catherine L. ; Li, Jinliang ; Matheson, Christopher J. ; Dodge-Kafka, Kimberly ; Reigan, Philip ; Kapiloff, Michael S. / RSK3 : A regulator of pathological cardiac remodeling. In: IUBMB Life. 2015 ; Vol. 67, No. 5. pp. 331-337.
@article{da7dfdba15d8419a9c6b8e279d0afe25,
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.",
keywords = "heart, hypertrophy, mAKAP, remodeling, ribosomal S6 kinase, scaffold, signal transduction",
author = "{Martinez Valencia}, {Eliana Cecilia} and Passariello, {Catherine L.} and Jinliang Li and Matheson, {Christopher J.} and Kimberly Dodge-Kafka and Philip Reigan and Kapiloff, {Michael S}",
year = "2015",
month = "5",
day = "1",
doi = "10.1002/iub.1383",
language = "English (US)",
volume = "67",
pages = "331--337",
journal = "IUBMB Life",
issn = "1521-6543",
publisher = "Wiley-Blackwell",
number = "5",

}

TY - JOUR

T1 - RSK3

T2 - A regulator of pathological cardiac remodeling

AU - Martinez Valencia, Eliana Cecilia

AU - Passariello, Catherine L.

AU - Li, Jinliang

AU - Matheson, Christopher J.

AU - Dodge-Kafka, Kimberly

AU - Reigan, Philip

AU - Kapiloff, Michael S

PY - 2015/5/1

Y1 - 2015/5/1

N2 - 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.

AB - 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.

KW - heart

KW - hypertrophy

KW - mAKAP

KW - remodeling

KW - ribosomal S6 kinase

KW - scaffold

KW - signal transduction

UR - http://www.scopus.com/inward/record.url?scp=84930208003&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84930208003&partnerID=8YFLogxK

U2 - 10.1002/iub.1383

DO - 10.1002/iub.1383

M3 - Article

VL - 67

SP - 331

EP - 337

JO - IUBMB Life

JF - IUBMB Life

SN - 1521-6543

IS - 5

ER -