The Role of Na/K-ATPase Signaling in Oxidative Stress Related to Aging: Implications in Obesity and Cardiovascular Disease

Bartlett, David E.; Miller, Richard B.; Thiesfeldt, Scott; Lakhani, Hari Vishal; Shapiro, Joseph I.; Sodhi, Komal

doi:10.3390/ijms19072139

Cited by 42 publications

(37 citation statements)

References 81 publications

(114 reference statements)

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“…Regarding ion channel dysregulation, Na + /K + exchangers appeared upregulated in all aging models and more strikingly in old WT mice. This alteration has been reported to promote oxidative stress in the aging heart (Bartlett et al, 2018). Lastly, in relation to signaling pathways, our studies show that calcium, G‐protein, and cAMP signaling proteins are differently dysregulated in the progeric and normal aging models.…”

Section: Discussionmentioning

confidence: 90%

Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging

et al. 2020

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Section: Discussionmentioning

confidence: 90%

Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging

et al. 2020

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“…Therefore, the mechanistic action of cardiotonic steroids may further stimulate the synthesis of cholesterol in NAFLD, which may lead to the activation of hepatic stellate cells, substantially aggravating hepatic fibrosis or lipid accumulation [26][27][28][29][30] and redox inflammatory pathways [31][32][33][34]. The cumulative line of evidence also suggests the role of cardiotonic steroids in the activation of Na/K-ATPase signaling [35][36][37][38]. Na/K-ATPase signaling has been extensively shown to have signaling and scaffolding functions, distinct from its cellular ion pumping function [39].…”

Section: Introductionmentioning

confidence: 99%

Predicting Nonalcoholic Fatty Liver Disease through a Panel of Plasma Biomarkers and MicroRNAs in Female West Virginia Population

Pillai

Lakhani

Zehra

et al. 2020

IJMS

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(1) Background: Nonalcoholic fatty liver disease (NAFLD) is primarily characterized by the presence of fatty liver, hepatic inflammation and fibrogenesis eventually leading to nonalcoholic steatohepatitis (NASH) or cirrhosis. Obesity and diabetes are common risk factors associated with the development and progression of NAFLD, with one of the highest prevalence of these diseased conditions in the West Virginia population. Currently, the diagnosis of NAFLD is limited to radiologic studies and biopsies, which are not cost-effective and highly invasive. Hence, this study aimed to develop a panel and assess the progressive levels of circulatory biomarkers and miRNA expression in patients at risk for progression to NASH to allow early intervention strategies. (2) Methods: In total, 62 female patients were enrolled and blood samples were collected after 8–10 h of fasting. Computed tomography was performed on abdomen/pelvis following IV contrast administration. The patients were divided into the following groups: Healthy subjects with normal BMI and normal fasting blood glucose (Control, n = 20), Obese with high BMI and normal fasting blood glucose (Obese, n = 20) and Obese with high fasting blood glucose (Obese + DM, n = 22). Based on findings from CT, another subset was created from Obese + DM group with patients who showed signs of fatty liver infiltration (Obese + DM(FI), n = 10). ELISA was performed for measurement of plasma biomarkers and RT-PCR was performed for circulating miRNA expression. (3) Results: Our results show significantly increased levels of plasma IL-6, Leptin and FABP-1, while significantly decreased level of adiponectin in Obese, Obese + DM and Obese + DM(FI) group, as compared to healthy controls. The level of CK-18 was significantly increased in Obese + DM(FI) group as compared to control. Subsequently, the expression of miR-122, miR-34a, miR-375, miR-16 and miR-21 was significantly increased in Obese + DM and Obese + DM(FI) group as compared to healthy control. Our results also show distinct correlation of IL-6, FABP-1 and adiponectin levels with the expression of miRNAs in relation to the extent of NAFLD progression. (4) Conclusion: Our results support the clinical application of these biomarkers and miRNAs in monitoring the progression of NAFLD, suggesting a more advanced diagnostic potential of this panel than conventional methods. This panel may provide an appropriate method for early prognosis and management of NAFLD and subsequent adverse hepatic pathophysiology, potentially reducing the disease burden on the West Virginia population.

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“…e term "oxidative stress" implies a physiological imbalance in the ROS creation and scavenging. Inflammation, which is triggered by oxidative stress, is associated with many diseases, such as oral ulcers [5], neurodegenerative diseases [6], tumour [7,8], cardiovascular disease [9,10], type 2 diabetes [11], nonalcoholic fatty liver disease [12], and Parkinson's disease [13]. Since it has been recognized that antioxidants can alleviate inflammatory reactions, some antioxidants have been studied and proposed for therapeutic use based on their therapeutic effects [14], e.g., vitamin C, coenzyme Q10, and some polyphenols that are isolated from herbs [15].…”

Section: Introductionmentioning

confidence: 99%

Zhibaidihuang Decoction Ameliorates Cell Oxidative Stress by Regulating the Keap1‐Nrf2‐ARE Signalling Pathway

Ding

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Zhibaidihuang decoction (ZBDHD) is a Chinese herbal formula, which is used in Chinese traditional medicine to treat symptoms of Yinxuhuowang (Yin deficiency and high fire) syndrome. This study elucidates the mechanism of ZBDHD on oral ulcers, one Yinxuhuowang syndrome. Simultaneously, some ingredients in ZBDHD were found and identified by ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). A Ganjiangfuzirougui decoction- (GJD-) induced Yinxuhuowang syndrome SD rat model was used to demonstrate the efficiency of ZBDHD treatment. The oral mucosa of rat in the GJD group, stained with hematoxylin and eosin (H&E), showed epidermal shedding and inflammatory cell infiltration. And an alleviation efficiency of ZBDHD in GJD-induced pathological changes in the oral mucosa could be obtained. ZBDHD treatment restored the GJD-induced imbalance of metabolites, which were choline, glycocholic acid, and palmitoyl-L-carnitine (PALC). GJD stimulated the expression of NF-κB. And the overexpressed of NF-κB in mucosa of rat in the GJD group could be inhibited by ZBDHD treatment. Simultaneously, the optimal efficiency of ZBDHD treatment on the cellular ATP content, oxygen consumption rate (OCR), and superoxide dismutase (SOD) concentration was evaluated, in vitro assay. Compared to the control cells, the ATP content, OCR, and SOD activity in the ZBDHD-treated cells were significantly higher. For the mechanisms study, seven cytokines were screened with a Dual-Luciferase Reporter gene assay. In the ARE assay, the luciferase signal was stimulated significantly by ZBDHD. In cells, the transcription of nrf2, maf, and keap1, which were related to the ARE pathway, was elevated by ZBDHD treatment. Our study demonstrated that high-dose GJD could lead to Yinxuhuowang syndrome, such as oral ulcers, and the imbalance in serum metabolites. And ZBDHD can improve oral cell inflammation and the imbalance of metabolism by inhibiting NF-κB and enhancing the activity of the ARE signalling pathway to ameliorate oxidative stress in the cell. This study provides a theoretical basis for the clinical application of ZBDHD.

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The Role of Na/K-ATPase Signaling in Oxidative Stress Related to Aging: Implications in Obesity and Cardiovascular Disease

Cited by 42 publications

References 81 publications

Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging

Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging

Predicting Nonalcoholic Fatty Liver Disease through a Panel of Plasma Biomarkers and MicroRNAs in Female West Virginia Population

Zhibaidihuang Decoction Ameliorates Cell Oxidative Stress by Regulating the Keap1‐Nrf2‐ARE Signalling Pathway

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