Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients

Li, Ting-Bo; Zhang, Yinzhuang; Liu, Weiqi; Zhang, Jie; Peng, Jun; Luo, Xiu-Ju; Ma, Qin

doi:10.3904/kjim.2016.140

Cited by 19 publications

(11 citation statements)

References 29 publications

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“…Lipid toxicity is an important cause of metabolic cardiomyopathy in rodents and humans ( Li et al, 2018 ). Hypertriglyceridemia causes abnormalities in the intake and circulating levels of FFA as well as abnormal degrees of oxidation ( Li et al, 2018 ), ultimately inducing pathological changes, such as myocardial cell apoptosis ( Yang et al, 2014 ). Many studies have suggested that cardiomyocyte apoptosis is closely related to impaired myocardial function.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Nanoparticles Attenuate Lipotoxic Injury in Cardiomyocytes Through Autophagy and Endoplasmic Reticulum Stress Signaling Pathways

Xia

Chen

et al. 2021

Front. Pharmacol.

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Although curcumin (CUR) has many advantages, its hydrophobicity and instability limit its application. In this study, the anti-lipotoxic injury activity of CUR-loaded nanoparticles (CUR-NPs) and the corresponding mechanism were examined in palmitate (PA)-treated cardiomyocytes. An amphiphilic copolymer was selected as the vehicle material, and CUR-NPs with suitable sizes were prepared under optimized conditions. Cellular uptake was examined by confocal laser scanning microscopy, and cell proliferation inhibition rate was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra bromide (MTT) assay. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was used to detect cell apoptosis. The protein expression was detected by western blot. Exposure to PA reduces the proliferation of cardiomyocytes, but this effect was strongly reversed by CUR-NPs. In addition, our data showed that CUR-NPs strongly inhibited cell apoptosis in PA-treated cardiomyocytes. Furthermore, CUR-NPs remarkably increased the expression of LC3-II, as well as inhibited the expression of p-PERK, p-eIF2α, and ATF4 in PA-treated cardiomyocytes. Salubrinal (an eIF2α inhibitor) blocked the protective effect of CUR-NPs against PA-induced cardiomyocyte injury. Our results suggested that CUR-NPs can activated the autophagy pathway and protect myocardial cells from apoptosis, and these effects may be mediated by the eIF2α-related endoplasmic reticulum stress signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Curcumin Nanoparticles Attenuate Lipotoxic Injury in Cardiomyocytes Through Autophagy and Endoplasmic Reticulum Stress Signaling Pathways

Xia

Chen

et al. 2021

Front. Pharmacol.

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“…Although the study involved only a small number of people (30 hyperlipidemic patients and 30 age-matched volunteers), the results showed an increase in NOX expression (NOX2 and NOX4), NOX activity, and consequently ROS production in hyperlipidemic patients, leading to a reduction in EPC functions. This positive correlation between the NOX-mediated oxidative stress and the dysfunctions of circulating EPCs in hyperlipidemic patients suggests that the inhibition and/or downregulation of NOX might be useful as novel strategy to improve EPC functions in hyperlipidemia [ 164 ]. The same research group previously obtained similar results in a rat model [ 165 ].…”

Section: Noxs In Endothelial Progenitors: Effect On Cell Survival Proliferation and Angiogenic Functionmentioning

confidence: 99%

NADPH Oxidases: Redox Regulators of Stem Cell Fate and Function

et al. 2021

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One of the major sources of reactive oxygen species (ROS) generated within stem cells is the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes (NOXs), which are critical determinants of the redox state beside antioxidant defense mechanisms. This balance is involved in another one that regulates stem cell fate: indeed, self-renewal, proliferation, and differentiation are decisive steps for stem cells during embryo development, adult tissue renovation, and cell therapy application. Ex vivo culture-expanded stem cells are being investigated for tissue repair and immune modulation, but events such as aging, senescence, and oxidative stress reduce their ex vivo proliferation, which is crucial for their clinical applications. Here, we review the role of NOX-derived ROS in stem cell biology and functions, focusing on positive and negative effects triggered by the activity of different NOX isoforms. We report recent findings on downstream molecular targets of NOX-ROS signaling that can modulate stem cell homeostasis and lineage commitment and discuss the implications in ex vivo expansion and in vivo engraftment, function, and longevity. This review highlights the role of NOX as a pivotal regulator of several stem cell populations, and we conclude that these aspects have important implications in the clinical utility of stem cells, but further studies on the effects of pharmacological modulation of NOX in human stem cells are imperative.

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“…NOX4-derived ROS production has been implicated in endothelial dysfunction and inflammation during obesity [167,168]. Evidence has shown that miR-25 is expressed in ECs [169].…”

Section: Oxidative Stress and Mirnasmentioning

confidence: 99%

MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy

Ait‐Aissa¹,

Nguyen²,

Gabani³

et al. 2020

Cardiovasc Diabetol

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The endothelium plays a pivotal role in maintaining vascular health. Obesity is a global epidemic that has seen dramatic increases in both adult and pediatric populations. Obesity perturbs the integrity of normal endothelium, leading to endothelial dysfunction which predisposes the patient to cardiovascular diseases. MicroRNAs (miRNAs) are short, single-stranded, non-coding RNA molecules that play important roles in a variety of cellular processes such as differentiation, proliferation, apoptosis, and stress response; their alteration contributes to the development of many pathologies including obesity. Mediators of obesity-induced endothelial dysfunction include altered endothelial nitric oxide synthase (eNOS), Sirtuin 1 (SIRT1), oxidative stress, autophagy machinery and endoplasmic reticulum (ER) stress. All of these factors have been shown to be either directly or indirectly caused by gene regulatory mechanisms of miRNAs. In this review, we aim to provide a comprehensive description of the therapeutic potential of miRNAs to treat obesity-induced endothelial dysfunction. This may lead to the identification of new targets for interventions that may prevent or delay the development of obesity-related cardiovascular disease.

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Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients

Cited by 19 publications

References 29 publications

Curcumin Nanoparticles Attenuate Lipotoxic Injury in Cardiomyocytes Through Autophagy and Endoplasmic Reticulum Stress Signaling Pathways

Curcumin Nanoparticles Attenuate Lipotoxic Injury in Cardiomyocytes Through Autophagy and Endoplasmic Reticulum Stress Signaling Pathways

NADPH Oxidases: Redox Regulators of Stem Cell Fate and Function

MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy

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