Endothelium-Derived Nitric Oxide as an Antiatherogenic Mechanism:
                        Implications for Therapy

Sukhovershin, Roman; Yepuri, Gautham; Ghebremariam, Yohannes T.

doi:10.14797/mdcj-11-3-166

Cited by 43 publications

(35 citation statements)

References 48 publications

(47 reference statements)

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“…Several pathogenic mechanisms by which PPIs may directly affect the risk of major adverse cardiovascular events have been proposed. Nitric oxide (NO) causes vasodilation and reduces platelet aggregation, which is essential for cardiovascular homoeostasis . Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of NO synthase .…”

Section: Discussionmentioning

confidence: 99%

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Batchelor

Kumar

Gilmartin‐Thomas

et al. 2018

Aliment Pharmacol Ther

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Section: Discussionmentioning

confidence: 99%

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Batchelor

Kumar

Gilmartin‐Thomas

et al. 2018

Aliment Pharmacol Ther

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“…The agonistinduced dephosphorylation of eNOS-Thr 495 in the calmodulin-binding domain is entirely Ca 2+ -dependent [42,46]. Hypoxia, erythropoietin, oxidized low-density lipoprotein, and inflammatory stimuli affect eNOS gene expression and stability [47]. eNOS mostly targets the caveolae of the plasma membrane [48].…”

Section: The Effects Of Agiv On the Pi3k/akt/enos Signaling Pathwaymentioning

confidence: 99%

Astragaloside IV Improves Vasodilatation Function by Regulating the PI3K/Akt/eNOS Signaling Pathway in Rat Aorta Endothelial Cells

et al. 2018

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Coronary heart disease (CHD) remains a major public health burden. Endothelial-dependent coronary artery vasoreactivity is a significant indicator of vascular function. Endothelial dysfunction is characterized by decreased nitric oxide (NO) bioavailability and predicts late cardiovascular events. Astragaloside IV (AGIV) is the main active component of the herb Astragalus membranaceus. Although it shows a significant protective effect against vascular endothelial dysfunction, the mechanisms of AGIV promoting the vascular dilation have not been elucidated. This study investigated the vasodilator effect of AGIV on rat aortic rings and the underlying effect of AGIV via the PI3K/Akt/eNOS signaling pathway. We measured the relaxation of isolated RARs after different concentrations of AGIV treatment. Rat aorta endothelial cells were cultured with different doses of AGIV, dimethylsulfoxide, and NG-nitro L-arginine methyl ester. The expression of phosphorylated (p)-Akt and -endothelial nitric oxide synthase (p-eNOS) were tested by Western blot analysis. The messenger (m)RNA expression of eNOS was quantified by real-time polymerase chain reaction. AGIV exerted a vasodilator effect on the aortic rings and increased the NO content in a concentration-dependent manner. The vasorelaxation was suppressed by an eNOS inhibitor. AGIV regulated the PI3K/Akt/eNOS signaling pathway via phosphorylation of Akt at Ser⁴⁷³ and dephosphorylation of eNOS at Thr⁴⁹⁵. The mRNA expression of eNOS was remarkably upregulated by AGIV. AGIV significantly induced the dilation of the aortic rings, leading to the vasodilator response by enhancing the eNOS release via the PI3K/Akt/eNOS signaling pathway.

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“…eNOS, neuronal NOS (nNOS), and inducible NOS (iNOS) are three isoforms of NOS. eNOS and nNOS are expressed under a physiological condition, while iNOS is highly expressed under a pathological condition . Ox‐LDL, as an important trigger of AS, has been reported to induce endothelial dysfunction via reducing eNOS activity and NO level .…”

Section: Discussionmentioning

confidence: 90%

“…eNOS and nNOS are expressed under a physiological condition, while iNOS is highly expressed under a pathological condition. 25 Ox-LDL, as an important trigger of AS, has been reported to induce endothelial dysfunction via reducing eNOS activity and NO level. 24,26 A previous study demonstrated that icariin could prohibit atherogenesis by increasing NO concentration and eNOS expression.…”

Section: Discussionmentioning

confidence: 99%

Golgi apparatus fragmentation participates in oxidized low‐density lipoprotein‐induced endothelial cell injury

Song

Wang

et al. 2019

J of Cellular Biochemistry

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Oxidized low‐density lipoprotein (ox‐LDL)‐induced endothelial injury plays crucial roles in the development of arteriosclerosis (AS). Golgi apparatus (GA) fragmentation is involved in various pathological processes, including endothelial injury. However, the role of GA fragmentation in ox‐LDL‐induced endothelial injury has not been determined. In this study, human umbilical vein endothelial cells (HUVECs) subjected to ox‐LDL were used as an in vitro AS model. Herein, we showed that ox‐LDL restrained proliferation and induced apoptosis and GA fragmentation of HUVECs. Moreover, overexpression of GRASP65 significantly prevented ox‐LDL‐induced GA fragmentation and endothelial cell injury by enhancing cell viability, nitric oxide production, and endothelial NOS expression and reducing apoptosis. Mechanistically, ox‐LDL resulted in the activation of the extracellular signal‐regulated kinase (ERK) pathway in HUVECs. Inactivation of the ERK pathway by U0126 suppressed the phosphorylation of GRASP65, GA fragmentation, and endothelial cell injury induced by ox‐LDL. In conclusion, ox‐LDL triggers GA fragmentation in HUVECs via activating the ERK signaling pathway, which participates in endothelial injury during the development of AS.

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Endothelium-Derived Nitric Oxide as an Antiatherogenic Mechanism: Implications for Therapy

Cited by 43 publications

References 48 publications

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Systematic review with meta‐analysis: risk of adverse cardiovascular events with proton pump inhibitors independent of clopidogrel

Astragaloside IV Improves Vasodilatation Function by Regulating the PI3K/Akt/eNOS Signaling Pathway in Rat Aorta Endothelial Cells

Golgi apparatus fragmentation participates in oxidized low‐density lipoprotein‐induced endothelial cell injury

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