Anti-hypoxic effect of dihydroartemisinin on pulmonary artery endothelial cells

Hua, Yu; Liu, Jingjing; Dong, Yizhi; Xu, Min; Xu, Le; Guan, Huaqin; Xia, Xiaoru; Wang, Liangxing

doi:10.1016/j.bbrc.2018.10.176

Cited by 16 publications

(20 citation statements)

References 37 publications

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“…Dihydroartemisinin (DHA), an agent that has anti-inflammatory, anti-malaria, and anti-tumor effects has been shown to reduce the symptoms of MCT-induced PH. DHA inhibits pulmonary arterial EC proliferation and reduces oxidative stress by increasing SOD expression and reducing ROS (Yu et al, 2018). PPARα agonist fenofibrate (FF) is another discovered therapy against oxidative stress and PH.…”

Section: Targeting Oxidative Stress In Rv Remodeling Associated With mentioning

confidence: 99%

Oxidative Stress and Its Implications in the Right Ventricular Remodeling Secondary to Pulmonary Hypertension

et al. 2019

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Pulmonary hypertension (PH) is a pulmonary vascular disease characterized by increased pulmonary artery pressures. Long standing pulmonary arterial pressure overload leads to right ventricular (RV) hypertrophy, RV failure, and death. RV failure is a major determinant of survival in PH. Oxidative stress has been associated with the development of RV failure secondary to PH. Here we summarize the structural and functional changes in the RV in response to sustained pulmonary arterial pressure overload. Furthermore, we review the pre-clinical and clinical studies highlighting the association of oxidative stress with pulmonary vasculature and RV remodeling in chronic PH. Targeting oxidative stress promises to be an effective therapeutic strategy for the treatment of RV failure.

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Section: Targeting Oxidative Stress In Rv Remodeling Associated With mentioning

confidence: 99%

Oxidative Stress and Its Implications in the Right Ventricular Remodeling Secondary to Pulmonary Hypertension

et al. 2019

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“…This predication is supported by results indicating that miR-30a-5p overexpression promoted cell proliferation and inhibited apoptosis of HPAECs under hypoxia. Hypoxia-induced HPAEC proliferation and inhibition of HPAEC proliferation is a strategy to attenuate the pathogenesis of PAH (26,27). PAH may also induce apoptosis-resistance in endothelial cells (28).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑30a‑5p promotes proliferation and inhibits apoptosis of human pulmonary artery endothelial cells under hypoxia by targeting YKL‑40

et al. 2019

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Pulmonary arterial hypertension (PAH) is a fatal and currently incurable cardiopulmonary disease. Numerous microRNAs (miRNAs) serve important roles in the development of PAH. While the expression of miR-30a-5p was downregulated in the lung tissue of rats in a pulmonary hypertension rat model, the expression pattern and function of miR-30a-5p in human PAH remain unclear. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to examine miR-30a-5p and chitinase-3-like protein 1 (YKL-40) mRNA expression levels. The expression levels of YKL-40 and apoptosis-associated proteins were measured by western blot analysis. Cell proliferation assays and flow cytometry analysis were performed to examine cell proliferation and apoptosis, respectively. The association between miR-30a-5p and YKL-40 was determined by a luciferase reporter assay, RT-qPCR and western blot analysis. The relative expression levels of miR-30a-5p in plasma were increased in patients with PAH [median=13.23 (25th percentile=6.388, 75th percentile=21.91)] compared with normal controls [median=2.25 (25th percentile=1.4, 75th percentile=3.7). The expression of miR-30a-5p was significantly downregulated while the protein expression of YKL-40 was significantly upregulated in hypoxia-induced human pulmonary artery endothelial cells (HPAECs) when compared with the hypoxia-induced group at 0 h. miR-30a-5p overexpression promoted HPAEC growth and inhibited apoptosis of HPAECs under hypoxia. A miR-30a-5p mimic decreased the luciferase activity of a luciferase reporter construct containing YKL-40 3′-untranslated region and also decreased YKL-40 protein expression. YKL-40 overexpression partly alleviated the effects of miR-30a-5p upregulation on proliferation and apoptosis of HPAECs under hypoxia. In conclusion, the data indicated that miR-30a-5p promoted cell growth and inhibited apoptosis of HPAECs under hypoxia by targeting YKL-40. Therefore, the miR-30a-5p/YKL-40 axis may provide a potential target for the development of novel PAH therapies.

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“…DHA blocks PAECs proliferation and diminishes OS by augmenting SOD expression and decreasing ROS in MCT-PH rats. 205 No clinical studies have yet been performed to investigate the effects of DHA in PAH subjects.…”

Section: Dihydroartemisinin (Dha)mentioning

confidence: 99%

Novel Experimental Therapies for Treatment of Pulmonary Arterial Hypertension

Zolty¹

2021

JEP

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Pulmonary arterial hypertension (PAH) is a progressive and devastating disease characterized by pulmonary artery vasoconstriction and vascular remodeling leading to vascular rarefaction with elevation of pulmonary arterial pressures and pulmonary vascular resistance. Often PAH will cause death from right heart failure. Current PAH-targeted therapies improve functional capacity, pulmonary hemodynamics and reduce hospitalization. Nevertheless, today PAH still remains incurable and is often refractory to medical therapy, underscoring the need for further research. Over the last three decades, PAH has evolved from a disease of unknown pathogenesis devoid of effective therapy to a condition whose cellular, genetic and molecular underpinnings are unfolding. This article provides an update on current knowledge and summarizes the progression in recent advances in pharmacological therapy in PAH.

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Anti-hypoxic effect of dihydroartemisinin on pulmonary artery endothelial cells

Cited by 16 publications

References 37 publications

Oxidative Stress and Its Implications in the Right Ventricular Remodeling Secondary to Pulmonary Hypertension

Oxidative Stress and Its Implications in the Right Ventricular Remodeling Secondary to Pulmonary Hypertension

MicroRNA‑30a‑5p promotes proliferation and inhibits apoptosis of human pulmonary artery endothelial cells under hypoxia by targeting YKL‑40

Novel Experimental Therapies for Treatment of Pulmonary Arterial Hypertension

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