Gastrin exerts a protective effect against myocardial infarction via promoting angiogenesis

Area of Science:

• Cardiovascular Research
• Endocrinology
• Regenerative Medicine

Background:

• Elevated gastrin levels correlate with reduced cardiovascular mortality.
• Plasma gastrin increases post-myocardial infarction (MI), but its role in MI protection is unclear.

Purpose of the Study:

• To investigate the protective effects of gastrin in a mouse model of myocardial infarction.
• To explore the underlying mechanisms of gastrin's action on cardiac function and angiogenesis.

Main Methods:

• Adult mice underwent LAD ligation to induce MI, followed by gastrin administration.
• Echocardiography assessed cardiac function; angiogenesis was evaluated via CD31 and VEGF expression.
• In vitro assays examined gastrin's effect on endothelial cell migration and tube formation, with CCK2R blockade used to confirm receptor involvement.

Main Results:

• Gastrin significantly improved cardiac function and reduced fibrosis in post-MI hearts.
• Gastrin decreased cardiomyocyte apoptosis and enhanced angiogenesis in the infarct border zone.
• Gastrin upregulated the PI3K/Akt/VEGF pathway, promoting endothelial cell activity, an effect mediated by the CCK2R.

Conclusions:

• Gastrin administration promotes angiogenesis and enhances cardiac function in a mouse model of MI.
• Gastrin's protective effects are mediated via the CCK2R and the PI3K/Akt/VEGF pathway.
• Gastrin represents a potential therapeutic target for improving outcomes after myocardial infarction.