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Endothelial dysfunction

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https://www.readbyqxmd.com/read/28635626/adiponectin-a-therapeutic-target-for-obesity-diabetes-and-endothelial-dysfunction
#1
REVIEW
Arunkumar E Achari, Sushil K Jain
Adiponectin is the most abundant peptide secreted by adipocytes, whose reduction plays a central role in obesity-related diseases, including insulin resistance/type 2 diabetes and cardiovascular disease. In addition to adipocytes, other cell types, such as skeletal and cardiac myocytes and endothelial cells, can also produce this adipocytokine. Adiponectin effects are mediated by adiponectin receptors, which occur as two isoforms (AdipoR1 and AdipoR2). Adiponectin has direct actions in liver, skeletal muscle, and the vasculature...
June 21, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28635612/consequences-of-lipopolysaccharide-and-n-3-polyunsaturated-fatty-acid-administration-on-aortic-function-of-spontaneously-hypertensive-rats
#2
Barbara Kaprinay, Ruzena Sotnikova, Karel Frimmel, Jakub Krizak, Iveta Bernatova, Jana Navarova, Ludmila Okruhlicova
The aim of the work was to study the delayed effect of lipopolysaccharide (LPS) administration on endothelial function of the aorta of rats with genetic hypertension. Further, the possibility to ameliorate LPS-induced changes by n-3 polyunsaturated fatty acids (n-3 PUFA) was tested. Rats received a bolus of 1 mg/kg LPS i.p.; n-3 PUFA were administered in the dose of 30 mg/kg daily for 10 days p.o.. Ten days after receiving of LPS, the body weight gain of rats was statistically lower compared to control rats (p < 0...
July 2017: General Physiology and Biophysics
https://www.readbyqxmd.com/read/28635324/gliptins-suppress-inflammatory-macrophage-activation-to-mitigate-inflammation-fibrosis-oxidative-stress-and-vascular-dysfunction-in-models-of-non-alcoholic-steatohepatitis-and-liver-fibrosis
#3
Xiaoyu Wang, Michael Hausding, Shih-Yen Weng, Yong Ook Kim, Sebastian Steven, Thomas Klein, Andreas Daiber, Detlef Schuppan
AIMS: Non-alcoholic steatohepatitis (NASH) is characterized by steatosis, panlobular inflammation, liver fibrosis and increased cardiovascular mortality. Dipeptidyl peptidase-4 (DPP-4) inhibitors (gliptins) are indirect glucagon like peptide 1 (GLP-1) agonists with antidiabetic and anti-inflammatory activity, used for the treatment of type 2 diabetes. Their potential and underlying mechanisms to treat metabolic liver inflammation and fibrosis as well as the associated vascular dysfunction remain to be explored...
June 21, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28634578/neonatal-venous-thromboembolism
#4
REVIEW
Kristina M Haley
Neonates are the pediatric population at highest risk for development of venous thromboembolism (VTE), and the incidence of VTE in the neonatal population is increasing. This is especially true in the critically ill population. Several large studies indicate that the incidence of neonatal VTE is up almost threefold in the last two decades. Central lines, fluid fluctuations, sepsis, liver dysfunction, and inflammation contribute to the risk profile for VTE development in ill neonates. In addition, the neonatal hemostatic system is different from that of older children and adults...
2017: Frontiers in Pediatrics
https://www.readbyqxmd.com/read/28634450/leonurine-improves-age-dependent-impaired-angiogenesis-possible-involvement-of-mitochondrial-function-and-hif-1%C3%AE-dependent-vegf-activation
#5
Jia Qi, Jing J Wang, Jun L Duan, Zhao Y Lu, Yang G Yuan
Objective: Advanced age is associated with impaired angiogenesis in part because of mitochondrial dysfunction. We have recently reported that leonurine exerts protective effects in neuron via regulation of mitochondrial function. The aim of this study was to explore whether leonurine is able to attenuate mitochondrial dysfunction and to enhance angiogenesis in old rats with hindlimb ischemia. Methods and Results: At day 14 after surgery, hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) expression was decreased in the ischemic muscle of aged animals, which was accompanied by enhanced oxidative stress, increased mitochondrial damage, decreased capillary density, and reduced limb perfusion compared with young mice...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28634267/30-years-of-the-mineralocorticoid-receptor-the-role-of-the-mineralocorticoid-receptor-in-the-vasculature
#6
REVIEW
Jennifer J DuPont, Iris Z Jaffe
Since the mineralocorticoid receptor (MR) was cloned 30 years ago, it has become clear that MR is expressed in extra-renal tissues, including the cardiovascular system, where it is expressed in all cells of the vasculature. Understanding the role of MR in the vasculature has been of particular interest as clinical trials show that MR antagonism improves cardiovascular outcomes out of proportion to changes in blood pressure. The last 30 years of research have demonstrated that MR is a functional hormone-activated transcription factor in vascular smooth muscle cells and endothelial cells...
July 2017: Journal of Endocrinology
https://www.readbyqxmd.com/read/28634176/impact-of-glycemic-variability-on-chromatin-remodeling-oxidative-stress-and-endothelial-dysfunction-in-type-2-diabetic-patients-with-target-hba1c-levels
#7
Sarah Costantino, Francesco Paneni, Rodolfo Battista, Lorenzo Castello, Giuliana Capretti, Sergio Chiandotto, Luigi Tanese, Giulio Russo, Dario Pitocco, Gaetano A Lanza, Massimo Volpe, Thomas F Lüscher, Francesco Cosentino
Intensive glycemic control (IGC) targeting HbA1c fails to show an unequivocal reduction of macrovascular complications in type 2 diabetes (T2D), however the underlining mechanisms remain elusive. Epigenetic changes are emerging as important mediators of cardiovascular damage and may play a role in this setting. This study investigates whether epigenetic regulation of the adaptor protein p66(Shc), a key driver of mitochondrial oxidative stress, contributes to persistent vascular dysfunction in T2D patients despite IGC...
June 20, 2017: Diabetes
https://www.readbyqxmd.com/read/28633109/endothelial-nlrp3-inflammasome-activation-and-arterial-neointima-formation-associated-with-acid-sphingomyelinase-during-hypercholesterolemia
#8
Saisudha Koka, Min Xia, Yang Chen, Owais M Bhat, Xinxu Yuan, Krishna M Boini, Pin-Lan Li
The NLRP3 inflammasome has been reported to be activated by atherogenic factors, whereby endothelial injury and consequent atherosclerotic lesions are triggered in the arterial wall. However, the mechanisms activating and regulating NLRP3 inflammasomes remain poorly understood. The present study tested whether acid sphingomyelinase (ASM) and ceramide associated membrane raft (MR) signaling platforms contribute to the activation of NLRP3 inflammasomes and atherosclerotic lesions during hypercholesterolemia. We found that 7-ketocholesterol (7-Keto) or cholesterol crystal (ChC) markedly increased the formation and activation of NLRP3 inflammasomes in mouse carotid arterial endothelial cells (CAECs), as shown by increased colocalization of NLRP3 with ASC or caspase-1, enhanced caspase-1 activity and elevated IL-1β levels, which were markedly attenuated by mouse Asm siRNA, ASM inhibitor- amitriptyline, and deletion of mouse Asm gene...
June 15, 2017: Redox Biology
https://www.readbyqxmd.com/read/28632534/administration-of-tetrahydrobiopterin-bh4-protects-the-renal-microcirculation-from-ischemia-and-reperfusion-injury
#9
Lokmane Rahmania, Diego Orbegozo, Fuhong Su, Fabio Silvio Taccone, Jean-Louis Vincent, Daniel De Backer
BACKGROUND: Abdominal aortic aneurysm surgery with suprarenal cross-clamping is often associated with renal injury. Although the mechanism underlying such injury is unclear, tissue ischemia and reperfusion, which induces endothelial dysfunction and decreases the availability of tetrahydrobiopterin (BH4), may play a role. We evaluated whether BH4 administration prevents renal ischemia/reperfusion injury in an animal model of aortic cross-clamping. METHODS: Nineteen anesthetized, mechanically ventilated, and invasively monitored adult sheep were randomized into 3 groups: sham animals (n = 5) that underwent surgical preparation but no aortic clamping; an ischemia/reperfusion group (n = 7), where the aorta was clamped above the renal arteries for 1 hour, and a BH4 group (n = 7), in which animals received 20 mg/kg of BH4 followed by aortic cross-clamp for 1 hour...
June 17, 2017: Anesthesia and Analgesia
https://www.readbyqxmd.com/read/28630660/npc-exs-alleviate-endothelial-oxidative-stress-and-dysfunction-through-the-mir-210-downstream-nox2-and-vegfr2-pathways
#10
Hua Liu, Jinju Wang, Yusen Chen, Yanfang Chen, Xiaotang Ma, Ji C Bihl, Yi Yang
We have demonstrated that neural progenitor cells (NPCs) protect endothelial cells (ECs) from oxidative stress. Since exosomes (EXs) can convey the benefit of parent cells through their carried microRNAs (miRs) and miR-210 is ubiquitously expressed with versatile functions, we investigated the role of miR-210 in the effects of NPC-EXs on oxidative stress and dysfunction in ECs. NPCs were transfected with control and miR-210 scramble/inhibitor/mimic to generate NPC-EXs(con), NPC-EXs(sc), NPC-EXs(anti-miR-210), and NPC-EXs(miR-210)...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28630659/homocysteine-induces-apoptosis-of-human-umbilical-vein-endothelial-cells-via-mitochondrial-dysfunction-and-endoplasmic-reticulum-stress
#11
Zhimin Zhang, Congying Wei, Yanfen Zhou, Tao Yan, Zhengqiang Wang, Wei Li, Lianyou Zhao
Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspase-3...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28630432/down-regulation-of-kca2-3-channels-causes-erectile-dysfunction-in-mice
#12
Simon Comerma-Steffensen, Attila Kun, Elise R Hedegaard, Susie Mogensen, Christian Aalkjaer, Ralf Köhler, Birgitte Mønster Christensen, Ulf Simonsen
Modulation of endothelial calcium-activated K(+) channels has been proposed as an approach to restore arterial endothelial cell function in disease. We hypothesized that small-conductance calcium-activated K(+) channels (KCa2.3 or SK3) contributes to erectile function. The research was performed in transgenic mice with overexpression (KCa2.3 (T/T(-Dox))) or down-regulation (KCa2.3 (T/T(+Dox))) of the KCa2.3 channels and wild-type C57BL/6-mice (WT). QPCR revealed that KCa2.3 and KCa1.1 channels were the most abundant in mouse corpus cavernosum...
June 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28630004/co-releasing-molecules-2-attenuates-ox-ldl-induced-injury-in-huvecs-by-ameliorating-mitochondrial-function-and-inhibiting-wnt-%C3%AE-catenin-pathway
#13
Hai-Jian Sun, Dong-Yan Xu, Yi-Xin Sun, Tong Xue, Chen-Xing Zhang, Zhi-Xuan Zhang, Wei Lin, Ke-Xue Li
Oxidized low-density lipoprotein (ox-LDL) is well known to disrupt normal functionality of endothelium, which plays a prominent role in endothelial dysfunction in many cardiovascular diseases. CO-releasing molecule 2 (CORM-2) is a promising candidate for treatment of cardiovascular diseases. However, it has not been defined whether CORM-2 might improve endothelial injury induced by ox-LDL. The present study was undertaken to determine the regulatory role of CORM-2 in cell injury of ox-LDL-treated human umbilical vein endothelial cells (HUVECs)...
June 16, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28628347/preventive-treatment-with-atorvastatin-ameliorates-endothelial-dysfunction-of-small-pulmonary-arteries-in-monocrotaline-induced-pulmonary-hypertensive-rats
#14
Zhihong Lin, Zhi Jiang, Xiaodong Huang, Xiaoqi Cai, Huajun Wang, Liangdi Xie
This study examined the effects of preventive atorvastatin (Ator) treatment on vasodilatation of small pulmonary arteries (SPAs) in monocrotaline (MCT)-induced pulmonary hypertensive rats. SD rats were randomly assigned to: normal control (Ctr), pulmonary arterial hypertension (PAH), PAH treated with 5 mg/kg/d Ator (LAtor), or 10 mg/kg/d Ator (HAtor). PAH was induced by MCT injection (40 mg/kg, i.p.). Mean pulmonary artery pressure (mPAP), right ventricular hypertrophy index (RVHI%), endothelium-dependent relaxations (EDdRs), and endothelium-independent relaxations (EDiRs) were determined...
June 19, 2017: Clinical and Experimental Hypertension: CHE
https://www.readbyqxmd.com/read/28628273/exposure-of-induced-pluripotent-stem-cell-derived-vascular-endothelial-and-smooth-muscle-cells-in-coculture-to-hemodynamics-induces-primary-vascular-cell-like-phenotypes
#15
Maria S Collado, Banumathi K Cole, Robert A Figler, Mark Lawson, David Manka, Michael B Simmers, Steve Hoang, Felipe Serrano, Brett R Blackman, Sanjay Sinha, Brian R Wamhoff
Human induced pluripotent stem cells (iPSCs) can be differentiated into vascular endothelial (iEC) and smooth muscle (iSMC) cells. However, because iECs and iSMCs are not derived from an intact blood vessel, they represent an immature phenotype. Hemodynamics and heterotypic cell:cell communication play important roles in vascular cell phenotypic modulation. Here we tested the hypothesis that hemodynamic exposure of iECs in coculture with iSMCs induces an in vivo-like phenotype. iECs and iSMCs were cocultured under vascular region-specific blood flow hemodynamics, and compared to hemodynamic cocultures of blood vessel-derived endothelial (pEC) and smooth muscle (pSMC) cells...
June 19, 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28628220/importance-of-endothelial-dysfunction-biomarkers-in-patients-with-crimean-congo-hemorrhagic-fever
#16
Mustafa Arslan, Gürdal Yilmaz, Ahmet Mentese, Hülya Yilmaz, S Caner Karahan, Iftihar Koksal
BACKGROUND: The pathogenesis of the Crimean-Congo hemorrhagic fever (CCHF) and the cause of the hemorrhage are not yet fully understood. However, the endothelium plays a key role in the pathogenesis. The purpose of this study was to investigate endothelial dysfunction markers [asymmetrical dimethyl arginine(ADMA), endothelin 1(ET-1), thrombomodulin(TM), von Willebrand factor(vWf) and intercellular adhesion molecule(ICAM-1)] in serum in patients with CCHF and their associations with hemorrhage...
June 19, 2017: Journal of Medical Virology
https://www.readbyqxmd.com/read/28627674/mir-200c-serves-an-important-role-in-h5v-endothelial-cells-in-high-glucose-by-targeting-notch1
#17
Yunfeng Zhang, Qiang Guan, Xing Jin
Diabetic vasculopathy is the leading cause of impairment and death in diabetic patients, a variety of factors are involved in its underlying pathological process, however, endothelial cell (EC) dysfunction serves a significant role in the process. MicroRNAs (miRNAs) have emerged as potential therapeutic candidates, due to their ability to regulate multiple targets involved in ECs. The aim of the present study was to investigate the role of miR‑200c in regulating ECs in high glucose condition. To investigate the role of miR‑200c in regulating hyperglycemia induced ECs by targeting Notch1, ECs H5V cells were cultured in high sugar conditions to initiate the inhibition of Notch1, the same cells in normal medium as the control...
June 15, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28627664/sodium-tanshinone-iia-sulfonate-suppresses-heat-stress-induced-endothelial-cell-apoptosis-by-promoting-no-production-through-upregulating-the-pi3k-akt-enos-pathway
#18
Qing Cheng, Yan Zhao, Jianguo Li
Heat shock is a life-threatening disease involving systematic inflammation that is closely related to endothelial injury and can lead to multiple organ dysfunction syndrome. Sodium tanshinone IIA sulfonate (STS) has various functions in the vascular endothelium. In the present study, STS is presented to suppress heat stress‑induced apoptosis of human umbilical vein endothelial cells (HUVECs) and high ambient temperature‑induced systematic inflammation in Sprague Dawley rats. In addition, the STS apoptosis‑suppression mechanism was explored...
June 13, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28627341/-protective-effects-of-valproic-acid-on-gut-barrier-function-after-major-burn-injury-and-its-mechanism
#19
Hongmin Luo, Sen Hu, Huining Bian, Shaoyi Zheng, Bing Xiong, Zhifeng Huang, Zuan Liu, Chuanwei Sun, Lianghua Ma, Hanhua Li, Wen Yu, Minghua Du, Huade Chen, Wen Lai
OBJECTIVE: To investigate the potential protective effects of valproic acid (VPA) on gut barrier function after major burn injury in rats and its mechanism. METHODS: Forty male Sprague-Dawley (SD) rats were divided into sham + normal saline (NS), sham + VPA, scald + NS, and scald + VPA groups, with 10 rats in each group. Rat with 55% total body surface area (TBSA) third-degree severe-burns model was reproduced by immersing into 80 °C water, and the rats in sham groups were given sham-burns by immersing into 37 °C water...
March 2017: Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
https://www.readbyqxmd.com/read/28626422/sphingosine-1-phosphate-receptors-do-they-have-a-therapeutic-potential-in-cardiac-fibrosis
#20
REVIEW
Ambra Vestri, Federica Pierucci, Alessia Frati, Lucia Monaco, Elisabetta Meacci
Sphingosine 1-phosphate (S1P) is a bioactive lipid that is characterized by a peculiar mechanism of action. In fact, S1P, which is produced inside the cell, can act as an intracellular mediator, whereas after its export outside the cell, it can act as ligand of specific G-protein coupled receptors, which were initially named endothelial differentiation gene (Edg) and eventually renamed sphingosine 1-phosphate receptors (S1PRs). Among the five S1PR subtypes, S1PR1, S1PR2 and S1PR3 isoforms show broad tissue gene expression, while S1PR4 is primarily expressed in immune system cells, and S1PR5 is expressed in the central nervous system...
2017: Frontiers in Pharmacology
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