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Updated: Aug 9, 2026

Transverse Aortic Constriction in Mice
08:25

Transverse Aortic Constriction in Mice

Published on: April 21, 2010

JNK1 is required to preserve cardiac function in the early response to pressure overload

Hideo Tachibana1, Cinzia Perrino, Hideyuki Takaoka

  • 1Department of Medicine, Cell Biology and Genetics, Duke University Medical Center, Durham, NC 27710, USA.

Biochemical and Biophysical Research Communications
|April 4, 2006
PubMed

Insights

Cardiac stress activates c-Jun NH(2)-terminal kinase (JNK) pathways. JNK1 deficiency impairs cardiac function during pressure overload, suggesting JNK1 has a protective role in the heart.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Stress Signaling

Background:

  • Cardiac stress activates c-Jun NH(2)-terminal kinase (JNK) pathways.
  • The specific roles of individual JNK family members in cardiac response to stress are not fully understood.

Purpose of the Study:

  • To investigate the distinct roles of JNK1, JNK2, and JNK3 in cardiac adaptation to pressure overload.

Main Methods:

  • Utilized JNK1, JNK2, and JNK3 knockout mouse models subjected to transverse aortic constriction (TAC).
  • Assessed cardiac hypertrophy, fractional shortening, and inflammatory markers post-TAC.

Main Results:

  • All JNK knockout mice developed cardiac hypertrophy comparable to wild-type (WT) mice.
  • JNK1 knockout mice showed reduced fractional shortening, increased apoptosis (TUNEL staining), and inflammation after TAC.
  • JNK1 knockout mice exhibited initial cardiac dysfunction followed by a slow recovery and eventual progression of dysfunction.

Conclusions:

  • JNK1 plays a critical protective role in the early stages of pressure overload.
  • JNK1 deficiency exacerbates cardiac dysfunction and inflammation following acute increases in afterload.

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