Related Experiment Video

Updated: Jun 22, 2026

Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
08:38

Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery

Published on: August 16, 2019

[Expression of PI3K/Akt signal pathway in acute myocardial ischemia]

Ruixia Song1, Yongmin Xiong, Qun Chen

  • 1Key Laboratory of Environment and Gene Related to Diseases, Medical College of Xi'an Jiaotong University, Ministry of Education, Xi'an 710061, China. song-ruixia@126.com

Wei Sheng Yan Jiu = Journal of Hygiene Research
|June 25, 2009
PubMed
Abstract

Insights

Acute myocardial ischemia (AMI) in rats elevates phosphorylated Akt (pAkt), Caspase-3, and p38 expressions in cardiac and somatic muscles, indicating pathway involvement in AMI pathogenesis. Akt expression remained unchanged.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Research

Context:

  • Acute myocardial ischemia (AMI) is a critical condition affecting heart muscle function.
  • The PI3K/Akt signaling pathway plays a crucial role in cellular survival and apoptosis.
  • Understanding molecular mechanisms in AMI is vital for developing therapeutic strategies.

Purpose:

  • To investigate the role of the PI3K/Akt signaling pathway in AMI.
  • To quantify the expression levels of key proteins, including phosphorylated Akt (pAkt), Akt, Caspase-3, and p38, in myocardial and somatic tissues of AMI rat models.

Summary:

  • AMI was induced in rats using isoprinosine (ISO), with physiological changes confirmed by electrocardiogram and hemodynamics.
  • Western blot analysis revealed significantly higher expressions of pAkt, Caspase-3, and p38 in both cardiac and somatic muscles of AMI rats compared to controls (P < 0.05).
  • Expression levels of Akt did not show significant changes between AMI and normal rats (P = 0.477).

Impact:

  • The findings suggest that the PI3K/Akt pathway, particularly the activation of pAkt and downstream effectors like Caspase-3 and p38, is implicated in the pathophysiology of AMI.
  • This study provides insights into the molecular alterations occurring in both cardiac and peripheral tissues during AMI.
  • Identifying these molecular changes can pave the way for targeted interventions to mitigate AMI-induced damage.

More Related Videos

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury07:23

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion13:42

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

Published on: July 17, 2012

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...