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Updated: Aug 14, 2026

Acute Myocardial Infarction in Rats
07:45

Acute Myocardial Infarction in Rats

Published on: February 16, 2011

p38 mitogen activated protein kinase mediates both death signaling and functional depression in the heart

Meijing Wang1, Ben M Tsai, Mark W Turrentine

  • 1Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana, USA.

The Annals of Thoracic Surgery
|November 25, 2005
PubMed
Abstract

Insights

Inhibiting p38 mitogen-activated protein kinase (MAPK) improves heart function after ischemia. This pathway is key in myocardial apoptosis and inflammation, suggesting p38 MAPK as a therapeutic target for heart protection.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Cellular Signaling

Background:

  • Myocardial inflammation following ischemia is crucial for long-term heart protection.
  • p38 mitogen-activated protein kinase (MAPK) is linked to oxidant stress-induced tumor necrosis factor production in the heart.
  • The role of p38 MAPK in mediating myocardial apoptosis and functional depression, including caspase and cytokine activation, remained unclear.

Purpose of the Study:

  • To investigate whether p38 MAPK mediates key events in myocardial apoptosis and functional depression.
  • To determine if p38 MAPK inhibition affects caspase activation and inflammatory cytokine production post-ischemia.

Main Methods:

  • Isolated rat hearts underwent ischemia-reperfusion insult.
  • Hearts were treated with or without a p38 MAPK inhibitor (SB203580).
  • Myocardial function, inflammatory markers (TNF, IL-1β, IL-6), and caspase activation (caspase-1, -3, -11) were assessed.

Main Results:

  • p38 MAPK inhibition significantly improved post-ischemic recovery of left ventricular pressure and contractility.
  • Inhibition reduced elevated left ventricular end-diastolic pressure.
  • p38 MAPK inhibition decreased levels of tumor necrosis factor, interleukin-1β, interleukin-6, and active caspases-1, -3, and -11.

Conclusions:

  • The p38 MAPK pathway is confirmed to mediate myocardial apoptosis and functional depression after ischemia.
  • p38 MAPK activation drives the production of inflammatory cytokines and activation of caspases.
  • Targeting p38 MAPK offers a potential therapeutic strategy for myocardial protection.

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