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The Role Played by Transcription Factor E3 in Modulating Cardiac Hypertrophy.

Ahmed Rishiq1, Omedul Islam2, Eliahu Golomb3

  • 1Department of Biochemistry and Molecular Biology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School.

International Heart Journal
|November 8, 2021
PubMed
Summary

Transcription factor E3 (TFE3) is crucial in cardiac hypertrophy. Its increased expression in heart disease suggests a role in the TFE3-histone-MYH7-pERK signaling pathway, impacting heart function.

Keywords:
CardioprotectionERK signalingMiceTransverse aortic constriction

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • Transcription factor E3 (TFE3) regulates cellular adaptation and is implicated in cardiac hypertrophy.
  • TFE3 expression is elevated in cardiac hypertrophy, but its precise role remains unclear.

Purpose of the Study:

  • To investigate the role of TFE3 in pressure-overload-induced cardiac hypertrophy.
  • To elucidate the molecular mechanisms by which TFE3 influences cardiac function and hypertrophy.

Main Methods:

  • Induction of pressure-overload cardiac hypertrophy via transverse aortic constriction (TAC) in wild-type and TFE3 knockout mice.
  • Assessment of cardiac function (ejection fraction, fractional shortening) and molecular markers (Myh7, ERK phosphorylation) in mouse models and human heart tissues.
  • In vitro studies using H9c2 cell line to explore TFE3-ERK interactions and downstream effects.

Main Results:

  • TFE3 knockout mice exhibited preserved cardiac function compared to wild-type mice after TAC.
  • TFE3 knockout mice showed reduced Myh7 expression and increased ERK phosphorylation post-TAC.
  • TFE3, histone, and MYH7 were upregulated, while pERK was downregulated in hypertensive human hearts and TFE3-manipulated cells.

Conclusions:

  • TFE3 expression is increased in cardiac hypertrophy, suggesting a detrimental role.
  • TFE3 appears to mediate cardiac hypertrophy through a signaling cascade involving histone, MYH7, and pERK.
  • Targeting the TFE3-histone-MYH7-pERK pathway may offer therapeutic potential for cardiac hypertrophy.