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https://www.readbyqxmd.com/read/27910925/thrombomodulin-regulates-monocye-differentiation-via-pkc%C3%AE-and-erk1-2-pathway-in-vitro-and-in-atherosclerotic-artery
#1
Chien-Sung Tsai, Yi-Wen Lin, Chun-Yao Huang, Chun-Min Shih, Yi-Ting Tsai, Nai-Wen Tsao, Chin-Sheng Lin, Chun-Che Shih, Hellen Jeng, Feng-Yen Lin
Thrombomodulin (TM) modulates the activation of protein C and coagulation. Additionally, TM regulates monocyte migration and inflammation. However, its role on monocyte differentiation is still unknown. We investigated the effects of TM on monocyte differentiation. First, we found that TM was increased when THP-1 cells were treated with phorbol-12-myristate-13-acetate (PMA). Overexpression of TM enhanced the macrophage markers, CD14 and CD68 expression in PMA-induced THP-1. TM siRNA depressed the PMA-induced increase of p21(Cip1/WAF1) via ERK1/2-NF-kB p65 signaling...
December 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27905479/role-of-gut-microbiota-in-atherosclerosis
#2
REVIEW
Annika Lindskog Jonsson, Fredrik Bäckhed
Infections have been linked to the development of cardiovascular disease and atherosclerosis. Findings from the past decade have identified microbial ecosystems residing in different habitats of the human body that contribute to metabolic and cardiovascular-related disorders. In this Review, we describe three pathways by which microbiota might affect atherogenesis. First, local or distant infections might cause a harmful inflammatory response that aggravates plaque development or triggers plaque rupture. Second, metabolism of cholesterol and lipids by gut microbiota can affect the development of atherosclerotic plaques...
December 1, 2016: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/27888053/current-understanding-of-atherogenesis
#3
REVIEW
Richard A Brown, Eduard Shantsila, Chetan Varma, Gregory Y H Lip
Scientific understanding of atherogenesis is constantly developing. From Virchow's observations 160 years ago we now recognise the endothelial response to injury to as inflammatory, involved in all stages of atherosclerosis. Endothelial activation may cause reversible injury or dysfunction, or lead to irreparable damage. Indeed, early atherosclerosis is reversible. The introduction of genome-wide association testing has furthered the identification of potentially important genetic variants that help explain the heritability coronary artery disease as well as spontaneous cases of severe coronary artery disease in patients with otherwise minimal risk factors...
November 22, 2016: American Journal of Medicine
https://www.readbyqxmd.com/read/27877049/a-review-about-biomarkers-for-the-investigation-of-vascular-function-and-impairment-in-diabetes-mellitus
#4
REVIEW
Giuseppe Derosa, Pamela Maffioli
The aim of this review was to analyze the main biomarkers of vascular function and impairment in patients with type 2 diabetes. Medline, SCOPUS, Web of Science, and Google Scholar databases were searched. We concluded that proatherogenic adhesion molecules (soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, and soluble E selectin) and inflammatory cytokines (high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α) were elevated in type 2 diabetes mellitus...
2016: Vascular Health and Risk Management
https://www.readbyqxmd.com/read/27871915/inhibition-of-siglec-1-by-lentivirus-mediated-small-interfering-rna-attenuates-atherogenesis-in-apoe-deficient-mice
#5
Yi-Song Xiong, Ai-Lin Wu, Dong Mu, Juan Yu, Ping Zeng, Yi Sun, Jie Xiong
BACKGROUND: Siglec-1 is highly expressed on circulating monocytes and plaque macrophages in atherosclerotic patients, but the exact role of Siglec-1 in atherosclerosis has not been elucidated. METHODS: Lentiviral vector containing small interfering RNA targeting Siglec-1 (Lv-shSiglec-1) or control vector (Lv-shNC) were injected intravenously into 6-week old Apoe(-/-) mice. Then onset of atherosclerosis was observed. RESULTS: Siglec-1 was highly expressed in aortic plaques and it can be down-regulated by Lv-shSiglec-1 injection...
November 15, 2016: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/27871059/selective-p38%C3%AE-map-kinase-mapk14-inhibition-in-enzymatically-modified-ldl-stimulated-human-monocytes-implications-for-atherosclerosis
#6
Fei Cheng, Laura Twardowski, Sarah Fehr, Christoph Aner, Elke Schaeffeler, Thomas Joos, Thomas Knorpp, Bernhard Dorweiler, Stefan Laufer, Matthias Schwab, Michael Torzewski
The first ATP-competitive p38α MAPK/MAPK14 inhibitor with excellent in vivo efficacy and selectivity, skepinone-L, is now available. We investigated the impact of selective p38α MAPK/MAPK14 inhibition on enzymatically modified LDL (eLDL) stimulated human monocytes with its implications for atherosclerosis. Among the different p38 MAPK isoforms, p38α/MAPK14 was the predominantly expressed and activated isoform in isolated human peripheral blood monocytes. Moreover, eLDL colocalized with macrophages positive for p38α MAPK/MAPK14 in human carotid endarterectomy specimens...
November 8, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27870587/17%C3%AE-estradiol-enhances-vascular-endothelial-ets-1-mir-126-3p-expression-the-possible-mechanism-for-attenuation-of-atherosclerosis
#7
Ping Li, Jinzhi Wei, Xiaosa Li, Yang Cheng, Weiyu Chen, Yuhong Cui, Tommaso Simoncini, Zhengtian Gu, Jun Yang, Xiaodong Fu
CONTEXT: Endothelial microRNA 126 (miR-126) attenuates the development of atherosclerosis (AS). However, there is no evidence showing the role of miR-126 in estrogen's anti-atherogenic effects. OBJECTIVE: We hypothesized that 17β-estradiol (E2) modulates miR-126 expression, thus may improve endothelial function and retard AS development. DESIGN/SETTING/PARTICIPANTS: This was a prospective cohort study of 12 healthy regularly menstruating female volunteers aged 23-26 yr conducted at Guangzhou Medical University...
November 21, 2016: Journal of Clinical Endocrinology and Metabolism
https://www.readbyqxmd.com/read/27869741/isoliquiritigenin-attenuates-atherogenesis-in-apolipoprotein-e-deficient-mice
#8
Fen Du, Quzhen Gesang, Jia Cao, Mei Qian, Li Ma, Dongfang Wu, Hong Yu
Isoliquiritigenin (ISL) exhibits antioxidation and anti-inflammation activity. We sought to investigate the effects and mechanism of ISL on the development of atherosclerotic lesions in apolipoprotein E-deficient (apoE(-/-)) mice. Firstly, we determined that ISL reduced the mRNA levels of inflammatory factors interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and monocyte chemotactic protein-1 (MCP-1), while it increased the expression of several lipoprotein-related genes in peritoneal macrophages treated with lipopolysaccharide (LPS)...
November 18, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27865196/-browning-the-cardiac-and-peri-vascular-adipose-tissues-to-modulate-cardiovascular-risk
#9
REVIEW
Peter Aldiss, Graeme Davies, Rachel Woods, Helen Budge, Harold S Sacks, Michael E Symonds
Excess visceral adiposity, in particular that located adjacent to the heart and coronary arteries is associated with increased cardiovascular risk. In the pathophysiological state, dysfunctional adipose tissue secretes an array of factors modulating vascular function and driving atherogenesis. Conversely, brown and beige adipose tissues utilise glucose and lipids to generate heat and are associated with improved cardiometabolic health. The cardiac and thoracic perivascular adipose tissues are now understood to be composed of brown adipose tissue in the healthy state and undergo a brown-to-white transition i...
November 9, 2016: International Journal of Cardiology
https://www.readbyqxmd.com/read/27863895/paraoxonase-1-q192r-gene-polymorphism-coronary-heart-disease-and-the-risk-of-a-new-acute-coronary-event
#10
Efrén Martínez-Quintana, Fayna Rodríguez-González, José María Medina-Gil, Paloma Garay-Sánchez, Antonio Tugores
INTRODUCTION: Paraoxonase 1 (PON1) plays a major role in the oxidation of low density lipoprotein and in the prevention of coronary atherogenesis. In this context, coding region polymorphisms of PON1 gene, responsible for the enzyme activity, has become of interest as a marker for atherogenesis. METHODS: A study and follow-up was conducted on 529 patients with an acute coronary event in order to assess the association between the PON1 Q192R (rs662;A/G) polymorphism, the type of acute coronary syndrome, cardiovascular risk factors (arterial hypertension, diabetes mellitus, dyslipidaemia, and smoking), the extent and severity of coronary atherosclerosis, and the medium-term clinical follow-up...
November 15, 2016: Clínica e Investigación en Arteriosclerosis
https://www.readbyqxmd.com/read/27862220/7-dehydrocholesterol-7-dhc-but-not-cholesterol-causes-suppression-of-canonical-tgf-%C3%AE-signaling-and-is-likely-involved-in-the-development-of-atherosclerotic-cardiovascular-disease-ascvd
#11
Shuan Shian Huang, I-Hua Liu, Chun-Lin Chen, Jia-Ming Chang, Frank E Johnson, Jung San Huang
For several decades, cholesterol has been thought to cause ASCVD. Limiting dietary cholesterol intake has been recommended to reduce the risk of the disease. However, several recent epidemiological studies do not support a relationship between dietary cholesterol and/or blood cholesterol and ASCVD. Consequently, the role of cholesterol in atherogenesis is now uncertain. Much evidence indicates that TGF-β, an anti-inflammatory cytokine, protects against ASCVD and that suppression of canonical TGF-β signaling (Smad2-dependent) is involved in atherogenesis...
November 16, 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/27856455/map3k8-modulates-monocyte-state-and-atherogenesis-in-apoe-mice
#12
Carlos Sanz-Garcia, Ángela Sánchez, Constanza Contreras-Jurado, Carmela Cales, Cristina Barranquero, Marta Muñóz, Ramón Merino, Paula Escudero, Maria-Jesús Sanz, Jesús Osada, Ana Aranda, Susana Alemany
OBJECTIVE: Map3k8 (Cot/Tpl2) activates the MKK1/2-ERK1/2, MAPK pathway downstream from interleukin-1R, tumor necrosis factor-αR, NOD-2R, adiponectinR, and Toll-like receptors. Map3k8 plays a key role in innate and adaptive immunity and influences inflammatory processes by modulating the functions of different cell types. However, its role in atherogenesis remains unknown. In this study, we analyzed the role of this kinase in this pathology. APPROACH AND RESULTS: We show here that Map3k8 deficiency results in smaller numbers of Ly6C(high)CD11c(low) and Ly6C(low)CD11c(high) monocytes in ApoE(-)(/-) mice fed a high-fat diet (HFD)...
November 17, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27847551/caspase-3-deletion-promotes-necrosis-in-atherosclerotic-plaques-of-apoe-knockout-mice
#13
Mandy O J Grootaert, Dorien M Schrijvers, Marthe Hermans, Viviane O Van Hoof, Guido R Y De Meyer, Wim Martinet
Apoptosis of macrophages and vascular smooth muscle cells (VSMCs) in advanced atherosclerotic plaques contributes to plaque progression and instability. Caspase-3, a key executioner protease in the apoptotic pathway, has been identified in human and mouse atherosclerotic plaques but its role in atherogenesis is not fully explored. We therefore investigated the impact of caspase-3 deletion on atherosclerosis by crossbreeding caspase-3 knockout (Casp3(-/-)) mice with apolipoprotein E knockout (ApoE(-/-)) mice...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27845432/protein-inhibitor-of-activated-stat3-suppresses-oxidized-ldl-induced-cell-responses-during-atherosclerosis-in-apolipoprotein-e-deficient-mice
#14
Rong Wang, Yanjin Zhang, Liran Xu, Yan Lin, Xiaofeng Yang, Liang Bai, Yulong Chen, Sihai Zhao, Jianglin Fan, Xianwu Cheng, Enqi Liu
Atherosclerosis is a serious public health concern. Excessive inflammatory responses of vascular cells are considered a pivotal pathogenesis mechanism underlying atherosclerosis development. It is known that Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signalling plays an important role in atherosclerosis progression. Protein inhibitor of activated STAT3 (PIAS3) is the key negative regulator of JAK/STAT3 signalling. However, its effect on atherogenesis is unknown. Here, we observed that PIAS3 levels are reduced in atherosclerotic lesions and that PIAS3 expression decreases in conjunction with increases in interleukin-6 expression and atherosclerosis severity...
November 15, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27843203/mir-155-regulated-inflammation-response-by-the-socs1-stat3-pdcd4-axis-in-atherogenesis
#15
Jinshan Ye, Ruiwei Guo, Yankun Shi, Feng Qi, Chuanming Guo, Lixia Yang
Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also found that miR-155 and PDCD4 were elevated in the aortic tissue of atherosclerotic mice and ox-LDL treated RAW264.7 cells. Further studies showed that miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-α...
2016: Mediators of Inflammation
https://www.readbyqxmd.com/read/27835742/silencing-of-cd40-in%C3%A2-vivo-reduces-progression-of-experimental-atherogenesis-through-an-nf-%C3%AE%C2%BAb-mir-125b-axis-and-reveals-new-potential-mediators-in-the-pathogenesis-of-atherosclerosis
#16
Miguel Hueso, Laura De Ramon, Estanislao Navarro, Elia Ripoll, Josep M Cruzado, Josep M Grinyo, Joan Torras
BACKGROUND AND AIMS: CD40/CD40L signaling exerts a critical role in the development of atherosclerosis, and microRNAs (miRNAs) are key regulators in vascular inflammation and plaque formation. In this work, we investigated mRNA/miRNA expression during progression of atherosclerotic lesions through CD40 silencing. METHODS: We silenced CD40 with a specific siRNA in ApoE(-/-) mice and compared expression of mRNA/miRNA in ascending aorta with scrambled treated mice...
November 2, 2016: Atherosclerosis
https://www.readbyqxmd.com/read/27834690/rac2-modulates-atherosclerotic-calcification-by-regulating-macrophage-interleukin-1%C3%AE-production
#17
Nicolle Ceneri, Lina Zhao, Bryan D Young, Abigail Healy, Suleyman Coskun, Hema Vasavada, Timur O Yarovinsky, Kenneth Ike, Ruggero Pardi, Lingfen Qin, Li Qin, George Tellides, Karen Hirschi, Judith Meadows, Robert Soufer, Hyung J Chun, Mehran Sadeghi, Jeffrey R Bender, Alan R Morrison
OBJECTIVE: The calcium composition of atherosclerotic plaque is thought to be associated with increased risk for cardiovascular events, but whether plaque calcium itself is predictive of worsening clinical outcomes remains highly controversial. Inflammation is likely a key mediator of vascular calcification, but immune signaling mechanisms that promote this process are minimally understood. APPROACH AND RESULTS: Here, we identify Rac2 as a major inflammatory regulator of signaling that directs plaque osteogenesis...
November 10, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27834689/nicotine-accelerates-atherosclerosis-in-apolipoprotein-e-deficient-mice-by-activating-%C3%AE-7-nicotinic-acetylcholine-receptor-on-mast-cells
#18
Chen Wang, Han Chen, Wei Zhu, Yinchuan Xu, Ming-Fei Liu, Lian-Lian Zhu, Fan Yang, Ling Zhang, Xian-Bao Liu, Zhiwei Zhong, Jing Zhao, Jun Jiang, Meixiang Xiang, Hong Yu, Xinyang Hu, Hong Lu, Jian'an Wang
OBJECTIVE: Cigarette smoking is an independent risk factor for atherosclerosis. Nicotine, the addictive component of cigarettes, induces mast cell (MC) release and contributes to atherogenesis. The purpose of this study was to determine whether nicotine accelerates atherosclerosis through MC-mediated mechanisms and whether MC stabilizer prevents this pathological process. APPROACH AND RESULTS: Nicotine administration increased the size of atherosclerotic lesions in apolipoprotein E-deficient (Apoe(-/-)) mice fed a fat-enriched diet...
November 10, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27822682/the-different-facets-of-dyslipidemia-and-hypertension-in-atherosclerosis
#19
REVIEW
Jessica Hurtubise, Krystie McLellan, Kevin Durr, Oluwadara Onasanya, Daniel Nwabuko, Joseph Fomusi Ndisang
Atherosclerosis is the narrowing of arteries due to the accumulation of macrophages overloaded with lipids resulting in foam cell formation, and these events occur preferentially at the branching points of arteries which are particularly susceptible to hyperlipidemic stress-induced inflammation and oxidative stress. The different stages of atherogenesis rely on oxidative stress, endothelial dysfunction, and inflammation, and hypertension or dyslipidemia can independently trigger these stages. Dyslipidemia and hypertension are pathological conditions that damage the endothelium, triggering cell proliferation, vascular remodeling, apoptosis, and increased cellular permeability with increased adhesion molecules that bind monocytes and T lymphocytes to create a vicious cocktail of pathophysiological factors...
December 2016: Current Atherosclerosis Reports
https://www.readbyqxmd.com/read/27821559/sex-steroids-block-the-initiation-of-atherosclerosis
#20
Frederick Naftolin, Holly Mehr, Ahmed Fadiel
Atherosclerosis is the main cause of death in men and women. This so-called "hardening of the arteries" results from advanced atherogenesis, the accumulation and death of subendothelial fat-laden macrophages (vascular plaque). The macrophages are attracted as the result of signals from injured vessels recruiting and activating cells to quell the injury by inflammation. Among the recruited cells are circulating monocytes that may be captured by the formation of neural cell adhesion molecule (nCAM) tethers between the monocytes and vascular endothelium; the tethers are dependent on electrostatic binding between distal segments of apposed nCAM molecules...
December 2016: Reproductive Sciences
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