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NPA7: A Dual Receptor Activating Peptide That Inhibits Cardiac Oxidative Stress.

Xiaoyu Ma¹, Joute Chawngvawr Malsawmzuali¹, Dante G Moroni¹

¹Cardiorenal Research Laboratory, Department of Cardiovascular Medicine (Xiaoyu Ma, J.C.M., D.G.M., Xiao Ma, Y.Z., S.P., Y.W., S.J.S., J.C.B.), Mayo Clinic, Rochester, MN.

Hypertension (Dallas, Tex. : 1979)

|January 8, 2025

Summary

Novel peptide NPA7 reduces oxidative stress in heart cells and hypertensive rats by activating antioxidant pathways. This peptide targets the GC-A/cGMP and MasR/cAMP pathways, offering a potential therapy for cardiovascular disease.

Keywords:

antioxidants cyclic AMP cyclic GMP hypertension oxidative stress

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Published on: June 11, 2020

Area of Science:

Cardiovascular Research
Molecular Biology
Pharmacology

Background:

Cardiomyocyte oxidative stress exacerbates hypertension-induced heart failure.
Targeted therapies are crucial for managing this condition.
A novel peptide, NPA7, was developed to coactivate GC-A/cGMP and MasR/cAMP pathways.

Purpose of the Study:

To investigate NPA7's antioxidant effects in human cardiomyocytes (HCMs) and a rat hypertension model.
To determine if NPA7 modulates the p62-KEAP1-NRF2 pathway.
To explore the role of GC-A, MasR, and p62 in NPA7's mechanism of action.

Main Methods:

Oxidative stress induced in HCMs with H2O2; treatment with NPA7.
Assessed reactive oxygen species (ROS) using dihydroethidium staining.
Western blotting for p62, KEAP1, NRF2; measured GSH/GSSG ratios and antioxidant gene expression.
Utilized siRNA for GC-A, MasR, p62 knockdown in HCMs.
In vivo study with spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats, measuring cardiac oxidative stress and related gene/protein levels.

Main Results:

NPA7 significantly reduced H2O2-induced ROS and increased GSH/GSSG ratio in HCMs.
Silencing GC-A or MasR abolished NPA7's protective effects.
NPA7 activated the KEAP1-NRF2 pathway, increasing antioxidant gene expression; p62 knockdown impaired this activation.
SHR hearts showed elevated ROS, which were reduced by NPA7 treatment.
NPA7 suppressed KEAP1 protein levels and decreased NOX2 and p67 mRNA in SHR hearts.

Conclusions:

NPA7 demonstrates potent antioxidant properties in both cellular and in vivo models of cardiovascular stress.
The peptide acts via the GC-A and MasR receptors, modulating the p62-KEAP1-NRF2 pathway.
NPA7 represents a promising therapeutic strategy for mitigating oxidative stress in cardiovascular diseases.