ArticleSleep & breathing = Schlaf & Atmung2023
The role of ferroptosis and endoplasmic reticulum stress in intermittent hypoxia-induced myocardial injury.
Article in Sleep & breathing = Schlaf & Atmung, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Ferroptosis in cardiovascular diseases: molecular mechanisms and a novel therapeutic target.Molecular biomedicine · 2026Review
- METTL3-m6A-SLC25A11 Axis Promotes Chronic Hypoxia-Induced Cardiomyocyte Ferroptosis.Journal of the American Heart Association · 2026Article
- Plumbagin Induces Ferroptosis in Nonfunctioning Pituitary Adenomas via Nrf2/FTH1-Dependent Ferritinophagy.Drug design, development and therapy · 2026Article
- Machine learning identifies potential diagnostic biomarkers associated with ferroptosis in obstructive sleep apnea.Experimental and therapeutic medicine · 2025Article
- In defence of ferroptosis.Signal transduction and targeted therapy · 2025Review
- Ferroptosis as a Potential Mechanism in the Pathophysiology of Obstructive Sleep Apnea Syndrome.Nature and science of sleep · 2025Review
- Manifold hepatoprotective actions of α-lipoic acid on metabolic function through redox regulation, inflammatory modulation, and anti-apoptosis after chronic sleep-deprived injury.Frontiers in nutrition · 2025Article
- Carvedilol Confers Ferroptosis Resistance in HL-1 Cells by Upregulating GPX4, FTH1, and FTL1 and Inducing Metabolic Remodeling Under Hypoxia/Reoxygenation.Antioxidants (Basel, Switzerland) · 2024Article
- Ferroptosis: mechanisms and therapeutic targets.MedComm · 2024Review
- Ferroptosis and endoplasmic reticulum stress in ischemic stroke.Neural regeneration research · 2024Review
- GDF15 restrains myocardial ischemia-reperfusion injury through inhibiting GPX4 mediated ferroptosis.Aging · 2024Article
- Chronic intermittent hypoxia aggravated diabetic cardiomyopathy through LKB1/AMPK/Nrf2 signaling pathway.PloS one · 2024Article
- Ferroptosis and myocardial ischemia-reperfusion: mechanistic insights and new therapeutic perspectives.Frontiers in pharmacology · 2024Review
- Exploring common biomarkers of ischemic stroke and obstructive sleep apnea through bioinformatics analysis.PloS one · 2024Article
- Targeting ferroptosis opens new avenues for the development of novel therapeutics.Signal transduction and targeted therapy · 2023Review
- Ferroptosis Regulated by Hypoxia in Cells.Cells · 2023Review
- Ferroptosis-related genes are considered as potential targets for CPAP treatment of obstructive sleep apnea.Frontiers in neurology · 2023Article
- Identification and validation of ferroptosis-related hub genes in obstructive sleep apnea syndrome.Frontiers in neurology · 2023Article
- Bioinformatics Analysis of Molecular Interactions between Endoplasmic Reticulum Stress and Ferroptosis under Stress Exposure.Analytical cellular pathology (Amsterdam) · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
purposeObstructive sleep apnea (OSA) is related to increased risk of cardiovascular disease. Ferroptosis is a form of programmed cell death characterized by iron overload and plays critical roles in myocardial injury. This study aimed to investigate the role of ferroptosis in intermittent hypoxia (IH)-induced myocardial injury involving endoplasmic reticulum stress (ERS).
methodsAC16 human cardiomyocytes were exposed to IH or normoxia conditions. Mice were randomly grouped as follows: normal control (NC), IH, ferrostatin-1 + IH (FIH), and N-acetylcysteine + IH (AIH). The mRNA levels of GPX4, xCT, FTH1, and FACL4 in AC16 cells were detected by qRT-PCR. The protein levels of GPX4, xCT, NOX4, ATF4, CHOP, Bcl-2, and Bax in myocardial tissue were detected by Western blot analysis.
resultsThe mRNA expression levels of GPX4 and xCT in AC16 cells were significantly lower in IH group than that of NC group. In IH mice, myocardial tissues were injured accompanied by increased level of ferroptosis and ERS. Inhibition of ferroptosis and treatment of N-acetylcysteine reduced ERS and myocardial injury in mice exposed to IH. In addition, compared to ferrostatin-1, N-acetylcysteine exerted a greater effect in relieving IH-induced myocardial damage and ERS.
conclusionsFerroptosis was involved in IH-related myocardial injury accompanied by the activation of ERS. Inhibition of ferroptosis and acetylcysteine treatment alleviated IH-related myocardial injury, which may be a potential target for therapeutic approaches to OSA-induced myocardial injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.