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ERK1/2: An Integrator of Signals That Alters Cardiac Homeostasis and Growth

Christopher J Gilbert1, Jacob Z Longenecker1, Federica Accornero1

  • 1Department of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.

Biology
|April 30, 2021
PubMed

Insights

Extracellular signal-regulated kinase (ERK) 1 and 2 are vital for heart cell survival and stress adaptation. This review details how ERK1/2 signaling impacts cardiac function and structure, especially in hypertrophy.

Area of Science:

  • Cardiovascular Biology
  • Cell Signaling
  • Molecular Cardiology

Background:

  • Cellular responses to external signals are crucial for survival and stress adaptation.
  • Extracellular signal-regulated kinase (ERK) 1 and 2 are key intracellular signal transducers in cardiomyocytes.
  • ERK1/2 signaling is critical for maintaining cardiac homeostasis and responding to stress.

Purpose of the Study:

  • To review the complex signaling pathways governing ERK1/2 activity in the heart.
  • To elucidate the role of ERK1/2 in regulating cardiac structure and function.
  • To emphasize the connection between ERK1/2 activation and cardiomyocyte hypertrophy.

Main Methods:

  • Literature review of studies on ERK1/2 signaling in the heart.
  • Analysis of upstream and downstream signaling components.
  • Focus on molecular mechanisms linking ERK1/2 to cardiac phenotypes.

Main Results:

  • ERK1/2 signaling is a central regulator of cardiomyocyte responses to stress.
  • Dysregulation of ERK1/2 pathways contributes to cardiac pathologies.
  • Cardiomyocyte hypertrophy is a significant outcome associated with altered ERK1/2 activation.

Conclusions:

  • Understanding ERK1/2 signaling is critical for comprehending normal cardiac function and disease.
  • Targeting ERK1/2 pathways may offer therapeutic strategies for heart conditions.
  • Further research into ERK1/2 regulation is essential for advancing cardiovascular medicine.
Keywords:
ERKcardiac hypertrophyextracellular matrixheart

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