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Post-myocardial infarction heart failure and long-term high-fat diet: Cardiac endoplasmic reticulum stress and unfolded protein response in Sprague Dawley rat model.
- Source :
-
PloS one [PLoS One] 2024 Sep 18; Vol. 19 (9), pp. e0308833. Date of Electronic Publication: 2024 Sep 18 (Print Publication: 2024). - Publication Year :
- 2024
-
Abstract
- Background: Myocardial infarction (MI) significantly contributes to the global mortality rate, often leading to heart failure (HF) due to left ventricular remodeling. Key factors in the pathomechanism of HF include nitrosative/oxidative stress, inflammation, and endoplasmic reticulum (ER) stress. Furthermore, while a high-fat diet (HFD) is known to exacerbate post-MI cardiac remodeling, its impact on these critical factors in the context of HF is not as well understood.<br />Aims: This study aimed to assess the impact of post-MI HF and HFD on inflammation, nitro-oxidative stress, ER stress, and unfolded protein response (UPR).<br />Methods: The study was performed on fragments of the left ventricle harvested from 30 male adult Sprague Dawley rats, which were divided into four groups based on diet (normal-fat vs. high-fat) and surgical procedure (sham operation vs. coronary artery ligation to induce MI). We assessed body weight, NT-proBNP levels, protein levels related to nitrosative/oxidative stress, ER stress, UPR, apoptosis, and nitric oxide synthases, through Western Blot and ELISA.<br />Results: HFD and MI significantly influenced body weight and NT-proBNP concentrations. HFD elevated 3-nitrotyrosine and myeloperoxidase levels and altered nitric oxide synthase levels. HFD and MI significantly affected ER stress markers and activated or inhibited UPR pathways.<br />Conclusions: The study demonstrates significant impacts of post-MI HF and dietary fat content on cardiac function and stress markers in a rat model. The interaction between HFD and MI on UPR activation suggests the importance of dietary management in post-MI recovery and HF prevention.<br />Competing Interests: The authors have declared that no competing interests exist.<br /> (Copyright: © 2024 Momot et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
- Subjects :
- Animals
Male
Rats
Disease Models, Animal
Apoptosis
Natriuretic Peptide, Brain metabolism
Peptide Fragments metabolism
Myocardium metabolism
Myocardium pathology
Myocardial Infarction metabolism
Myocardial Infarction pathology
Rats, Sprague-Dawley
Endoplasmic Reticulum Stress
Heart Failure metabolism
Heart Failure etiology
Heart Failure pathology
Diet, High-Fat adverse effects
Unfolded Protein Response
Oxidative Stress
Subjects
Details
- Language :
- English
- ISSN :
- 1932-6203
- Volume :
- 19
- Issue :
- 9
- Database :
- MEDLINE
- Journal :
- PloS one
- Publication Type :
- Academic Journal
- Accession number :
- 39292720
- Full Text :
- https://doi.org/10.1371/journal.pone.0308833