ArticlePloS one2014
Adiponectin alleviates genioglossal mitochondrial dysfunction in rats exposed to intermittent hypoxia.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 21 citations in OpenAlex.
- The Role of Mitochondria in Obstructive Sleep Apnea: Implications for the Upper Airway Muscles.International journal of molecular sciences · 2025Review
- Intermittent hypoxia induces myofibroblast differentiation and extracellular matrix production of MRC5s via HIF-1α-TGF-β/Smad pathway.Sleep & breathing = Schlaf & Atmung · 2024Article
- Chronic intermittent hypoxia aggravated diabetic cardiomyopathy through LKB1/AMPK/Nrf2 signaling pathway.PloS one · 2024Article
- Molecular Pathology, Oxidative Stress, and Biomarkers in Obstructive Sleep Apnea.International journal of molecular sciences · 2023Review
- Advances in Molecular Pathology of Obstructive Sleep Apnea.Molecules (Basel, Switzerland) · 2022Review
- Gestational Intermittent Hypoxia Induces Mitochondrial Impairment in the Geniohyoid Muscle of Offspring Rats.Cureus · 2022Article
- Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea.Frontiers in genetics · 2022Article
- The role of mitophagy in the mechanism of genioglossal dysfunction caused by chronic intermittent hypoxia and the protective effect of adiponectin.Sleep & breathing = Schlaf & Atmung · 2021Article
- How Does Chronic Intermittent Hypoxia Influence Upper Airway Stability in Rats?Nature and science of sleep · 2020Article
- Relationships Between Adipose Mitochondrial Function, Serum Adiponectin, and Insulin Resistance in Persons With HIV After 96 Weeks of Antiretroviral Therapy.Journal of acquired immune deficiency syndromes (1999) · 2019Article
- Adiponectin Relieves Human Adult Cardiac Myocytes Injury Induced by Intermittent Hypoxia.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Effect of different levels of intermittent hypoxia on autophagy of hippocampal neurons.Sleep & breathing = Schlaf & Atmung · 2017Article
- Respiratory muscle dysfunction in animal models of hypoxic disease: antioxidant therapy goes from strength to strength.Hypoxia (Auckland, N.Z.) · 2017Review
- Adiponectin protects the rats liver against chronic intermittent hypoxia induced injury through AMP-activated protein kinase pathway.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenioglossal dysfunction is involved in the pathophysiology of obstructive sleep apnea hypoxia syndrome (OSAHS) characterized by nocturnal chronic intermittent hypoxia (CIH). The pathophysiology of genioglossal dysfunction and possible targeted pharmacotherapy for alleviation of genioglossal injury in CIH require further investigation. METHODOLOGY/PRINCIPAL
findingsRats in the control group were exposed to normal air, while rats in the CIH group and CIH+adiponectin (AD) group were exposed to the same CIH condition (CIH 8 hr/day for 5 successive weeks). Furthermore, rats in CIH+AD group were administrated intravenous AD supplementation at the dosage of 10 µg, twice a week for 5 consecutive weeks. We found that CIH-induced genioglossus (GG) injury was correlated with mitochondrial dysfunction, reduction in the numbers of mitochondrias, impaired mitochondrial ultrastructure, and a reduction in type I fibers. Compared with the CIH group, impaired mitochondrial structure and function was significantly improved and a percentage of type I fiber was elevated in the CIH+AD group. Moreover, compared with the control group, the rats' GG in the CIH group showed a significant decrease in phosphorylation of LKB1, AMPK, and PGC1-α, whereas there was significant rescue of such reduction in phosphorylation within the CIH+AD group.
conclusionsCIH exposure reduces mitochondrial biogenesis and impairs mitochondrial function in GG, while AD supplementation increases mitochondrial contents and alleviates CIH-induced mitochondrial dysfunction possibly through the AMPK pathway.
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