Cardiovascular protection by ezetimibe and influence on oxidative stress in mice exposed to intermittent hypoxia

Kato, Ryuichi; Nishioka, Satoshi; Nomura, Atsuo; Ijiri, Yoshio; Miyamura, Masatoshi; Ukimura, Akira; Okada, Yoshinori; Kitaura, Yasushi; Hayashi, Toshio

doi:10.1016/j.ejphar.2015.08.013

Cited by 7 publications

(4 citation statements)

References 36 publications

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“…We found that the IH treatment resembling a moderate OSA condition led to left ventricular cardiac hypertrophy and contractile dysfunction, and the functional compromise was accompanied by structural impairment, that is interstitial fibrosis. These results are consistent with findings reported by us and other groups, showing IH‐induced ventricular remodelling and cardiac dysfunction …”

Section: Discussionsupporting

confidence: 94%

“…Once the balance of mitochondrial fission and fusion is disrupted, cardiomyocytes apoptosis consequently occurs and eventually leads to heart failure. Recent work has also shown that IH can cause mitochondrial abnormalities and myocardium interstitial fibrosis in apolipoprotein E‐knockout mice fed with high‐fat diet; however, it is still unclear whether the imbalance of mitochondrial fission and fusion plays a role in the pathological change in cardiac tissue. In current study, we showed that IH treatment increased mitochondrial fragmentation and cell apoptosis in NRCs and rat heart tissue, which were associated with enhanced expression of Drp1 and reduced expression of Mfn2.…”

Section: Discussionmentioning

confidence: 99%

“…These results are consistent with findings reported by us and other groups, showing IH-induced ventricular remodelling and cardiac dysfunction. 5,17,26,27 Apoptosis constitutes one of the major mechanisms acting as intermediary pathogenic links between OSA and cardiovascular disorders. Cardiomyocyte apoptosis contributes to cell loss followed by progressive myocardial dysfunction and the eventual heart failure.…”

Section: Discussionmentioning

confidence: 99%

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Haemin attenuates intermittent hypoxia‐induced cardiac injury via inhibiting mitochondrial fission

Han

Liu

et al. 2018

J Cellular Molecular Medi

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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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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Haemin attenuates intermittent hypoxia‐induced cardiac injury via inhibiting mitochondrial fission

Han

Liu

et al. 2018

J Cellular Molecular Medi

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“…Oxidative stress is one of the important causes of cardiovascular structural and functional abnormalities [ 40 ]. Studies have shown that the occurrence and development of cardiovascular diseases such as heart failure, arrhythmia, and cardiomyopathy are related to myocardial apoptosis [ 19 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

[Retracted] Protective Effect of a Novel Polysaccharide from Lonicera japonica on Cardiomyocytes of Mice Injured by Hydrogen Peroxide

Zhou

Tang³

et al. 2020

BioMed Research International

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Lonicera japonica is a traditional Chinese herbal medicine with antioxidation, anti-inflammatory, antibacterial, and immunoregulation functions. A method to isolate polysaccharides from Lonicera japonica (LJP) has been reported previously by our group. We also reported previously that LJP was consisted of 6 types of monosaccharides and had the characteristic absorption of typical polysaccharides. In this study, we investigated the protective effect of LJP on cardiomyocytes of mice injured by hydrogen peroxide (H2O2). The results showed that LJP can increase the cardiomyocyte viability and the activities of the enzyme (SOD, CAT, GSH-Px, AST, CPK, and LDH) in cardiomyocytes of mice injured by hydrogen peroxide. The results of intracellular ROS contents showed that a high dose (40 μg mL-1) of LJP had the best effects on protecting the cardiomyocytes of mice injured by H2O2. In addition, the measurement results of the cardiomyocyte apoptosis and the activity of caspase-3, caspase-8, and caspase-9 in cardiomyocytes confirmed this conclusion from another perspective.

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Long non-coding RNA H19, a negative regulator of microRNA-148b-3p, participates in hypoxia stress in human hepatic sinusoidal endothelial cells via NOX4 and eNOS/NO signaling

et al. 2019

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Cardiovascular protection by ezetimibe and influence on oxidative stress in mice exposed to intermittent hypoxia

Cited by 7 publications

References 36 publications

Haemin attenuates intermittent hypoxia‐induced cardiac injury via inhibiting mitochondrial fission

Haemin attenuates intermittent hypoxia‐induced cardiac injury via inhibiting mitochondrial fission

[Retracted] Protective Effect of a Novel Polysaccharide from Lonicera japonica on Cardiomyocytes of Mice Injured by Hydrogen Peroxide

Long non-coding RNA H19, a negative regulator of microRNA-148b-3p, participates in hypoxia stress in human hepatic sinusoidal endothelial cells via NOX4 and eNOS/NO signaling

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