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Updated: Feb 27, 2026
A Modified Simple Method for Induction of Myocardial Infarction in Mice
Published on: December 3, 2021
MAPK pathway regulated the cardiomyocyte apoptosis in mice with post-infarction heart failure
Background:
To explore the role of the MAPK signaling pathway in the cardiomyocyte apoptosis of mice with post-infarction heart failure (HF).
Methods:
Mice were divided into sham and myocardial infarction (MI) groups. Before surgery, the MI group was divided into SB203580 and PBS subgroups. A post-infarction HF model was established by ligating the left anterior descending coronary artery. Ventricular dilatation and cardiac function were observed by small animal echocardiography. The growth of primary cardiomyocytes was observed under an inverted phase contrast microscope. The mRNA and protein expressions of endoplasmic reticulum stress (ERS) markers, GRP78 and CHOP, were detected by qRT-PCR and immunofluorescence assay, respectively.
Results:
The MI group had enlarged left ventricle and decreased cardiac function. GRP78 and CHOP protein expressions in myocardial tissues, especially those of SB203580 subgroup, significantly increased (p < 0.05). The expressions of p-JNK and cleaved caspase 12 proteins, especially those of SB203580 subgroup, were significantly up-regulated. Cardiomyocytes of MI group were significantly more prone to apoptosis (p < 0.05), with SB203580 subgroup being more obvious.
Conclusion:
MI was accompanied by ERS, probably involving the MAPK signaling pathway. SB203580, a specific inhibitor of this pathway, can relieve cardiomyocyte apoptosis and protect the myocardium by suppressing such stress (Tab. 3, Fig. 7, Ref. 20).
Insights
Myocardial infarction triggers endoplasmic reticulum stress, leading to heart failure. Inhibiting the MAPK signaling pathway reduces cardiomyocyte apoptosis and protects the heart.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Signaling Pathways
Background:
- Post-infarction heart failure (HF) is characterized by cardiomyocyte apoptosis.
- The role of the MAPK signaling pathway in this process requires further elucidation.
Purpose of the Study:
- To investigate the involvement of the MAPK signaling pathway in cardiomyocyte apoptosis in a mouse model of post-infarction heart failure.
- To assess the therapeutic potential of inhibiting this pathway.
Main Methods:
- A mouse model of myocardial infarction (MI) was established.
- Mice were treated with SB203580 (a MAPK inhibitor) or PBS.
- Cardiac function, cardiomyocyte apoptosis, and endoplasmic reticulum stress (ERS) markers (GRP78, CHOP) were evaluated.
Main Results:
- MI led to ventricular dilatation and impaired cardiac function.
- ERS markers (GRP78, CHOP) and apoptosis markers (p-JNK, cleaved caspase 12) were significantly upregulated in MI hearts.
- SB203580 treatment attenuated these changes and reduced cardiomyocyte apoptosis.
Conclusions:
- Myocardial infarction induces endoplasmic reticulum stress, likely mediated by the MAPK signaling pathway.
- Inhibition of the MAPK pathway with SB203580 alleviates cardiomyocyte apoptosis and offers myocardial protection.
