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p53-Induced inflammation exacerbates cardiac dysfunction during pressure overload.

Yohko Yoshida1, Ippei Shimizu1, Goro Katsuumi2

  • 1Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan; Division of Molecular Aging and Cell Biology, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan.

Journal of Molecular and Cellular Cardiology
|June 10, 2015
PubMed
Summary

Severe heart failure remains a major health issue. This study reveals that p53-induced inflammation, driven by the sympathetic nervous system, worsens heart dysfunction, suggesting p53 inhibition as a potential therapy.

Keywords:
Bone marrow cellsEndothelial cellsHeart failureInflammation

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Inflammation Research

Background:

  • Severe heart failure is linked to high mortality and disability.
  • Sterile inflammation plays a key role in cardiac remodeling during heart failure.
  • The connection between p53 signaling and inflammation in heart failure is not well understood.

Purpose of the Study:

  • To investigate the role of p53-induced inflammation in the progression of heart failure.
  • To elucidate the link between the sympathetic nervous system, p53, and cardiac dysfunction.

Main Methods:

  • Examined p53 expression in cardiac cells and bone marrow cells under pressure overload.
  • Utilized genetic deletion and overexpression of p53 in relevant cell types.
  • Assessed the impact of norepinephrine and β2-adrenergic receptor modulation on cardiac function and inflammation.

Main Results:

  • Pressure overload increased p53 expression, leading to ICAM1 and integrin upregulation, cardiac inflammation, and systolic dysfunction.
  • p53 deletion in endothelial or bone marrow cells reduced inflammation and improved systolic function.
  • Sympathetic nervous system activation (norepinephrine) enhanced p53 expression and cardiac inflammation, exacerbating dysfunction.

Conclusions:

  • p53-induced inflammation, promoted by sympathetic nervous system activation, critically contributes to heart failure progression.
  • Targeting p53-mediated inflammation presents a potential therapeutic strategy for heart failure.