ArticleScientific reports2017
Chronic Intermittent Hypobaric Hypoxia Improves Cardiac Function through Inhibition of Endoplasmic Reticulum Stress.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Intermittent hypoxia reduces infarct size in rats with acute myocardial infarction: a systematic review and meta-analysis.BMC cardiovascular disorders · 2020Pooled it
- Cardiovascular risk and obesity in miner workers exposed to intermittent hypobaric hypoxia in the Peruvian Andes.Frontiers in physiology · 2026Article
- A new mechanism of high-altitude adaptation reducing myocardium infarction: inhibiting inflammation-induced ubiquitin degradation of BKBasic research in cardiology · 2025Article
- Article
- Hypoxia Acclimation Protects against Heart Failure Postacute Myocardial Infarction via Fundc1-Mediated Mitophagy.Oxidative medicine and cellular longevity · 2022Article
- Reactive Oxygen Species Regulate Endoplasmic Reticulum Stress and ER-Mitochondrial CaOxidative medicine and cellular longevity · 2021Article
- Intermittent Hypoxic Conditioning Alleviates Post-Traumatic Stress Disorder-Induced Damage and Dysfunction of Rat Visceral Organs and Brain.International journal of molecular sciences · 2020Article
- Chronic Intermittent Hypobaric Hypoxia Enhances Bone Fracture Healing.Frontiers in endocrinology · 2020Article
- Luteolin Attenuates Cardiac Ischemia/Reperfusion Injury in Diabetic Rats by Modulating Nrf2 Antioxidative Function.Oxidative medicine and cellular longevity · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the role of endoplasmic reticulum stress (ERS) in chronic intermittent hypobaric hypoxia (CIHH)-induced cardiac protection. Adult male Sprague-Dawley rats were exposed to CIHH treatment simulating 5000 m altitude for 28 days, 6 hours per day. The heart was isolated and perfused with Langendorff apparatus and subjected to 30-min ischemia followed by 60-min reperfusion. Cardiac function, infarct size, and lactate dehydrogenase (LDH) activity were assessed. Expression of ERS molecular chaperones (GRP78, CHOP and caspase-12) was assayed by western blot analysis. CIHH treatment improved the recovery of left ventricular function and decreased cardiac infarct size and activity of LDH after I/R compared to control rats. Furthermore, CIHH treatment inhibited over-expression of ERS-related factors including GRP78, CHOP and caspase-12. CIHH-induced cardioprotection and inhibition of ERS were eliminated by application of dithiothreitol, an ERS inducer, and chelerythrine, a protein kinase C (PKC) inhibitor. In conclusion CIHH treatment exerts cardiac protection against I/R injury through inhibition of ERS via PKC signaling pathway.
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