# Bioartificial Cardiac Patches Functionalized with Apelin-13 Increase Cardiac C-Type Natriuretic Peptide Expression in Infarcted Rats

## TL;DR

This study shows that patches treated with Apelin-13 can boost heart healing in rats with heart attacks by increasing a specific heart peptide.

## Contribution

The novel contribution is demonstrating that Apelin-13 functionalized patches modulate the CNP system in myocardial infarction.

## Key findings

- Apelin-13 patches reduced left ventricle wall thinning in infarcted rats.
- CNP mRNA expression was higher in infarcted groups, especially in the border/infarct zone.
- NPR-B receptor expression was higher in the remote zone compared to the border/infarct zone.

## Abstract

Background: recently, regenerative medicine has introduced a new branch of science that facilitates the repair of damaged tissues and organs in acute myocardial infarction. This study explores the role of the C-type natriuretic peptide (CNP) system in myocardial infarction (MI) and its modulation by Apelin-13 functionalized patches (A-13p). Methods: using an experimental rat model of ischemia/reperfusion, the rats were divided into four groups: Sham, Infarct, Sham with A-13p, and Infarct with A-13p. Cardiac tissue from the infarct, border, and remote zones was analyzed for CNP and its receptors’ mRNA expression via Real-Time PCR. Results: histological analysis, 4 weeks post A-13p implantation, showed no damage from A-13p implantation in either MI or Sham groups, with reduced left ventricle wall thinning in the Infarct group treated with A-13p. CNP mRNA expression was higher in the infarcted groups (p = ns), especially in the border/infarct zone (BZ + IZ), compared to the Sham group (p = 0.05). NPR-B receptor expression was higher in the RZ than in (BZ + IZ), both in the absence (p = 0.02) and presence of patches (p = 0.01), while NPR-C expression was lower. No significant differences were observed in VEGF mRNA levels across the groups. Conclusions: the findings suggest that the CNP system is involved in MI and that A-13p modulates CNP expression, highlighting CNP as a potential target for therapeutic strategies aimed at regulating vascular remodeling and angiogenesis in MI treatment.