ArticleJournal of cellular and molecular medicine2018
Haemin attenuates intermittent hypoxia-induced cardiac injury via inhibiting mitochondrial fission.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Mitochondrial dysfunction and oxidative stress in OSAHS and associated comorbidities: Mechanism and potential targeted therapeutic strategies.Redox biology · 2026Review
- PGC-1α: a potential therapeutic target for upper airway dilator muscle structure and dysfunction in OSA.Sleep & breathing = Schlaf & Atmung · 2025Review
- Obstructive sleep apnea and aging of the cardiovascular system: a multidimensional analysis of the mechanisms involved.Biogerontology · 2025Review
- Nr1d1 inhibition mitigates intermittent hypoxia-induced pulmonary hypertension via Dusp1-mediated Erk1/2 deactivation and mitochondrial fission attenuation.Cell death discovery · 2024Article
- Cytosolic Escape of Mitochondrial DNA Triggers cGAS-STING Pathway-Dependent Neuronal PANoptosis in Response to Intermittent Hypoxia.Neurochemical research · 2024Article
- Cardiomyocyte-specific overexpression of FPN1 diminishes cardiac hypertrophy induced by chronic intermittent hypoxia.Journal of cellular and molecular medicine · 2024Article
- Effects of obstructive sleep apnea on myocardial injury and dysfunction: a review focused on the molecular mechanisms of intermittent hypoxia.Sleep & breathing = Schlaf & Atmung · 2024Review
- Protective mechanisms of quercetin in neonatal rat brain injury induced by hypoxic-ischemic brain damage (HIBD).Food science & nutrition · 2023Article
- Cytoprotective Role of Heme Oxygenase-1 in Cancer Chemoresistance: Focus on Antioxidant, Antiapoptotic, and Pro-Autophagy Properties.Antioxidants (Basel, Switzerland) · 2023Review
- LncRNA XR_595552 inhibition alleviates intermittent hypoxia-induced cardiomyocyte damage via activating the PI3K/AKT pathway.Sleep & breathing = Schlaf & Atmung · 2023Article
- Mitochondria in hypoxic pulmonary hypertension, roles and the potential targets.Frontiers in physiology · 2023Review
- Ginsenoside Rg1 ameliorates chronic intermittent hypoxia-induced vascular endothelial dysfunction by suppressing the formation of mitochondrial reactive oxygen species through the calpain-1 pathway.Journal of ginseng research · 2023Article
- Cardioprotective Antioxidant and Anti-Inflammatory Mechanisms Induced by Intermittent Hypobaric Hypoxia.Antioxidants (Basel, Switzerland) · 2022Article
- Gestational Intermittent Hypoxia Induces Mitochondrial Impairment in the Geniohyoid Muscle of Offspring Rats.Cureus · 2022Article
- Mitochondrial Dynamics, Mitophagy, and Mitochondria-Endoplasmic Reticulum Contact Sites Crosstalk Under Hypoxia.Frontiers in cell and developmental biology · 2022Review
- Nesfatin-1 protects H9c2 cardiomyocytes against cobalt chloride-induced hypoxic injury by modulating the MAPK and Notch1 signaling pathways.Journal of biological research (Thessalonike, Greece) · 2021Article
- Early vs. Late Onset Cardiac Injury and Mortality in Hospitalized COVID-19 Patients in Wuhan.Frontiers in cardiovascular medicine · 2021Article
- HIF-1α ameliorates tubular injury in diabetic nephropathy via HO-1-mediated control of mitochondrial dynamics.Cell proliferation · 2020Article
- The role of reactive oxygen species in cognitive impairment associated with sleep apnea.Experimental and therapeutic medicine · 2020Article
- Haemin pre-treatment augments the cardiac protection of mesenchymal stem cells by inhibiting mitochondrial fission and improving survival.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obstructive sleep apnoea (OSA) characterized by intermittent hypoxia (IH) is closely associated with cardiovascular diseases. IH confers cardiac injury via accelerating cardiomyocyte apoptosis, whereas the underlying mechanism has remained largely enigmatic. This study aimed to explore the potential mechanisms involved in the IH-induced cardiac damage performed with the IH-exposed cell and animal models and to investigate the protective effects of haemin, a potent haeme oxygenase-1 (HO-1) activator, on the cardiac injury induced by IH. Neonatal rat cardiomyocyte (NRC) was treated with or without haemin before IH exposure. Eighteen male Sprague-Dawley (SD) rats were randomized into three groups: control group, IH group (PBS, ip) and IH + haemin group (haemin, 4 mg/kg, ip). The cardiac function was determined by echocardiography. Mitochondrial fission was evaluated by Mitotracker staining. The mitochondrial dynamics-related proteins (mitochondrial fusion protein, Mfn2; mitochondrial fission protein, Drp1) were determined by Western blot. The apoptosis of cardiomyocytes and heart sections was examined by TUNEL. IH regulated mitochondrial dynamics-related proteins (decreased Mfn2 and increased Drp1 expressions, respectively), thereby leading to mitochondrial fragmentation and cell apoptosis in cardiomyocytes in vitro and in vivo, while haemin-induced HO-1 up-regulation attenuated IH-induced mitochondrial fragmentation and cell apoptosis. Moreover, IH resulted in left ventricular hypertrophy and impaired contractile function in vivo, while haemin ameliorated IH-induced cardiac dysfunction. This study demonstrates that pharmacological activation of HO-1 pathway protects against IH-induced cardiac dysfunction and myocardial fibrosis through the inhibition of mitochondrial fission and cell apoptosis.
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