INOS contributes to heart failure with preserved ejection fraction through mitochondrial dysfunction and Akt S-nitrosylation.

ABSTRACT:

Introduction

Despite the high morbidity and mortality of heart failure with preserved fraction (HFpEF), there are currently no effective therapies for this condition. Moreover, the pathophysiological basis of HFpEF remains poorly understood.

Objective

The aim of the present study was to investigate the role of inducible nitric oxide synthase (iNOS) and its underlying mechanism in a high-fat diet and N^ω-nitro-L-arginine methyl ester-induced HFpEF mouse model.

Methods

The selective iNOS inhibitor L-NIL was used to examine the effects of short-term iNOS inhibition, whereas the long-term effects of iNOS deficiency were evaluated using iNOS-null mice. Cardiac and mitochondrial function, oxidative stress and Akt S-nitrosylation were then measured.

Results

SUBMITTER: Guo Y 

PROVIDER: S-EPMC9811328 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature