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macrophage and atherogenesis

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https://www.readbyqxmd.com/read/28765952/mtor-signaling-promotes-foam-cell-formation-and-inhibits-foam-cell-egress-through-suppressing-the-sirt1-signaling-pathway
#1
Haixiang Zheng, Yucai Fu, Yusheng Huang, Xinde Zheng, Wei Yu, Wei Wang
Atherosclerosis (AS) is a chronic immuno‑inflammatory disease accompanied by dyslipidemia. The authors previously demonstrated that sirtuin 1 (SIRT1) may prevent atherogenesis through influencing the liver X receptor/C‑C chemokine receptor type 7/nuclear factor‑κB (LXR‑CCR7/NF‑κB) signaling pathway. Previous studies have suggested a role for mammalian target of rapamycin (mTOR) signaling in the pathogenesis of cardiovascular diseases. The present study investigated the potential association between mTOR signaling and SIRT1‑LXR‑CCR7/NF‑κB signaling (SIRT1 signaling) in AS pathogenesis...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28760743/hypoxia-inducible-protein-2-hig2-hilpda-mediates-neutral-lipid-accumulation-in-macrophages-and-contributes-to-atherosclerosis-in-apolipoprotein-e-deficient-mice
#2
Anja Maier, Hao Wu, Nada Cordasic, Peter Oefner, Barbara Dietel, Christoph Thiele, Alexander Weidemann, Kai-Uwe Eckardt, Christina Warnecke
Recently we identified hypoxia-inducible protein 2 (HIG2)/hypoxia-inducible lipid droplet associated (HILPDA) as lipid droplet (LD) protein. Because HILPDA is highly expressed in atherosclerotic plaques, we examined its regulation and function in murine macrophages, compared it to the LD adipose differentiation-related protein (Adrp)/perilipin 2 (Plin2), and investigated its effects on atherogenesis in apolipoprotein E-deficient (ApoE(-/-)) mice. Tie2-Cre-driven Hilpda knockout (cKO) did not affect viability, proliferation, and ATP levels in macrophages...
July 31, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28743785/bubr1-insufficiency-results-in-decreased-macrophage-proliferation-and-attenuated-atherogenesis-in-apolipoprotein-e-deficient-mice
#3
(no author information available yet)
No abstract text is available yet for this article.
July 25, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28743735/lilrb4-deficiency-aggravates-the-development-of-atherosclerosis-and-plaque-instability-by-increasing-the-macrophage-inflammatory-response-via-nf-%C3%AE%C2%BAb-signaling
#4
Zhou Jiang, Juan-Juan Qin, Yaxing Zhang, Wen-Lin Cheng, Yan-Xiao Ji, Fu-Han Gong, Xue-Yong Zhu, Yan Zhang, Zhi-Gang She, Zan Huang, Hongliang Li
Atherosclerosis is a chronic inflammatory disease. LILRB4 is associated with the pathological processes of various inflammatory diseases. However, the potential function and underlying mechanisms of LILRB4 in atherogenesis remain to be investigated. In this study, LILRB4 expression was examined in both human and mouse atherosclerotic plaques. The effects and possible mechanisms of LILRB4 in atherogenesis and plaque instability were evaluated in LILRB4(-/-)ApoE(-/-) and ApoE(-/-) mice fed a high-fat diet. We found that LILRB4 was located primarily in macrophages, and its expression was up-regulated in atherosclerotic lesions from human coronary arteries and mouse aortic roots...
July 25, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28739472/toll-like-receptor-4-signaling-improved-the-migration-of-sca-1-stem-progenitor-cells
#5
Ying Huang, Chunya Zhang, Jinghua Shen, Xiaogang Zhang, Jianqing Du, Daifu Zhang
Atherosclerosis is considered as a chronic inflammatory process, during which macrophages and smooth muscle cells migrate into the vascular wall intima to initiate atherogenesis. Stem/progenitor cells (SPCs) have been demonstrated as a new source of monocytes/macrophages and smooth muscle cells (SMCs). However, the regulation of SPCs migration into atherosclerotic initiation sites to produce macrophages and SMCs in-situis not fully elucidated. As toll-like receptor (TLRs) signaling plays essential role in migration of immunocytes, we wanted to explore the expression and function of TLRs in SPCs in detail...
July 21, 2017: Annals of Vascular Surgery
https://www.readbyqxmd.com/read/28735290/membrane-tethered-metalloproteinase-expressed-by-vascular-smooth-muscle-cells-limits-the-progression-of-proliferative-atherosclerotic-lesions
#6
Richard H Barnes, Takeshi Akama, Miina K Öhman, Moon-Sook Woo, Julian Bahr, Stephen J Weiss, Daniel T Eitzman, Tae-Hwa Chun
BACKGROUND: The MMP (matrix metalloproteinase) family plays diverse and critical roles in directing vascular wall remodeling in atherosclerosis. Unlike secreted-type MMPs, a member of the membrane-type MMP family, MT1-MMP (membrane-type 1 MMP; MMP14), mediates pericellular extracellular matrix degradation that is indispensable for maintaining physiological extracellular matrix homeostasis. However, given the premature mortality exhibited by MT1-MMP-null mice, the potential role of the proteinase in atherogenesis remains elusive...
July 22, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28724798/hepatic-jak2-protects-against-atherosclerosis-through-circulating-igf-1
#7
Tharini Sivasubramaniyam, Stephanie A Schroer, Angela Li, Cynthia T Luk, Sally Yu Shi, Rickvinder Besla, David W Dodington, Adam H Metherel, Alex P Kitson, Jara J Brunt, Joshua Lopes, Kay-Uwe Wagner, Richard P Bazinet, Michelle P Bendeck, Clinton S Robbins, Minna Woo
Atherosclerosis is considered both a metabolic and inflammatory disease; however, the specific tissue and signaling molecules that instigate and propagate this disease remain unclear. The liver is a central site of inflammation and lipid metabolism that is critical for atherosclerosis, and JAK2 is a key mediator of inflammation and, more recently, of hepatic lipid metabolism. However, precise effects of hepatic Jak2 on atherosclerosis remain unknown. We show here that hepatic Jak2 deficiency in atherosclerosis-prone mouse models exhibited accelerated atherosclerosis with increased plaque macrophages and decreased plaque smooth muscle cell content...
July 20, 2017: JCI Insight
https://www.readbyqxmd.com/read/28674080/macrophage-deficiency-of-mir-21-promotes-apoptosis-plaque-necrosis-and-vascular-inflammation-during-atherogenesis
#8
Alberto Canfrán-Duque, Noemi Rotllan, Xinbo Zhang, Marta Fernández-Fuertes, Cristina Ramírez-Hidalgo, Elisa Araldi, Lidia Daimiel, Rebeca Busto, Carlos Fernández-Hernando, Yajaira Suárez
Atherosclerosis, the major cause of cardiovascular disease, is a chronic inflammatory disease characterized by the accumulation of lipids and inflammatory cells in the artery wall. Aberrant expression of microRNAs has been implicated in the pathophysiological processes underlying the progression of atherosclerosis. Here, we define the contribution of miR-21 in hematopoietic cells during atherogenesis. Interestingly, we found that miR-21 is the most abundant miRNA in macrophages and its absence results in accelerated atherosclerosis, plaque necrosis, and vascular inflammation...
July 3, 2017: EMBO Molecular Medicine
https://www.readbyqxmd.com/read/28642826/elucidation-of-the-role-of-lectin-like-oxldl-receptor-1-in-the-metabolic-responses-of-macrophages-to-human-oxldl
#9
Danielle W Kimmel, William P Dole, David E Cliffel
Atherogenesis is the narrowing of arteries due to plaque build-up that results in cardiovascular disease that can lead to death. The macrophage lectin-like oxidized LDL receptor-1 (LOX-1), also called the oxidized low-density lipoprotein receptor 1 (OLR1), is currently thought to aid in atherosclerotic disease progression; therefore metabolic studies have potential to both provide mechanistic validation for the role of LOX-1 in disease progression and provide valuable information regarding biomarker strategies and clinical imaging...
2017: Journal of Lipids
https://www.readbyqxmd.com/read/28641798/hiv-1-associated-atherosclerosis-unraveling-the-missing-link
#10
REVIEW
Alison Kearns, Jennifer Gordon, Tricia H Burdo, Xuebin Qin
Cardiovascular disease, including atherosclerosis and atherosclerosis-associated complications, is an increasing cause of morbidity and mortality in human immunodeficiency virus (HIV) patients in the post-antiretroviral therapy era. HIV alone accelerates atherosclerosis. Antiretroviral therapy; HIV-associated comorbidities, such as dyslipidemia, drug abuse, and opportunistic infections; and lifestyle are risk factors for HIV-associated atherosclerosis. However, our current understanding of HIV-associated atherogenesis is very limited and has largely been obtained from clinical observation...
June 27, 2017: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/28621675/the-regulation-of-immune-cells-by-lactobacilli-a-potential-therapeutic-target-for-anti-atherosclerosis-therapy
#11
REVIEW
Ya-Hui Ding, Lin-Yan Qian, Jie Pang, Jing-Yang Lin, Qiang Xu, Li-Hong Wang, Dong-Sheng Huang, Hai Zou
Atherosclerosis is an inflammatory disease regulated by several immune cells including lymphocytes, macrophages and dendritic cells. Gut probiotic bacteria like Lactobacilli have been shown immunomodificatory effects in the progression of atherogenesis. Some Lactobacillus stains can upregulate the activity of regulatory T-lymphocytes, suppress T-lymphocyte helper (Th) cells Th1, Th17, alter the Th1/Th2 ratio, influence the subsets ratio of M1/M2 macrophages, inhibit foam cell formation by suppressing macrophage phagocytosis of oxidized low-density lipoprotein, block the activation of the immune system with dendritic cells, which are expected to suppress the atherosclerosis-related inflammation...
June 2, 2017: Oncotarget
https://www.readbyqxmd.com/read/28615615/stat6-upregulation-promotes-m2-macrophage-polarization-to-suppress-atherosclerosis
#12
Min Gong, Xiaozhen Zhuo, Aiqun Ma
BACKGROUND Macrophages are highly heterogeneous and plastic cells that are involved in all stages of atherogenesis. They can undergo polarization by shifting between M1 and M2 functional phenotypes. However, the role of macrophage polarization and the molecular mechanism in modulating atherosclerotic plaque stability remain incompletely understood. Our study investigated the role of STAT6 in regulating macrophage phenotypes to affect atherosclerotic plaque stability. MATERIAL AND METHODS A murine atherosclerosis model with vulnerable plaques was induced with high-cholesterol diet and PCCP surgeries in ApoE-/- mice...
June 15, 2017: Medical Science Monitor Basic Research
https://www.readbyqxmd.com/read/28615349/cftr-protects-against-vascular-inflammation-and-atherogenesis-in-apolipoprotein-e-deficient-mice
#13
Zhengzhang Li, Zhe Shen, Haoping Xue, Shi Cheng, Qun Ji, Yutan Liu, Xiangjun Yang
Atherosclerosis is a chronic inflammatory disease of the vascular wall. Dysfunction of cystic fibrosis transmembrane conductance regulator (CFTR) has been shown to result in inflammatory responses in cystic fibrosis (CF) patients. However, little is known about the role of CFTR in vascular inflammation and atherogenesis. Our results showed that CFTR was dominantly expressed in macrophages of atherosclerotic plaque and reduced in aorta and aortic sinus from atherosclerotic apolipoprotein E-deficient (apoE-/-) mice...
June 14, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28615143/monocyte-macrophage-and-t-cell-activation-markers-are-not-independently-associated-with-mi-risk-in-healthy-individuals-results-from-the-hunt-study
#14
Thor Ueland, Lars E Laugsand, Lars J Vatten, Imre Janszky, Carl Platou, Annika E Michelsen, Jan K Damås, Pål Aukrust, Bjørn O Åsvold
BACKGROUND: We hypothesized that circulating markers reflecting monocyte/macrophage and T cell activation are associated with increased risk of myocardial infarction (MI) in apparently healthy individuals. METHODS: Serum monocyte/macrophage and T cell activation markers soluble (s) CD163, sCD14, Gal3BP, sCD25 and sCD166 were analyzed by enzyme-immunoassay in a case-control study nested within the population-based HUNT2 cohort in Norway. Among 58,761 apparently healthy men and women followed a median 11...
September 15, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28605287/prdx1-peroxiredoxin-1-deficiency-reduces-cholesterol-efflux-via-impaired-macrophage-lipophagic-flux
#15
Se-Jin Jeong, Sinai Kim, Jong-Gil Park, In-Hyuk Jung, Mi-Ni Lee, Sejin Jeon, Hyae Yon Kweon, Dae-Yeul Yu, Sang-Hak Lee, Yangsoo Jang, Sang Won Kang, Ki-Hwan Han, Yury I Miller, Young Mi Park, Cheolho Cheong, Jae-Hoon Choi, Goo Taeg Oh
Oxidative stress activates macroautophagy/autophagy and contributes to atherogenesis via lipophagic flux, a form of lipid removal by autophagy. However, it is not known exactly how endogenous anti-oxidant enzymes are involved in lipophagic flux. Here, we demonstrate that the anti-oxidant PRDX1 (peroxiredoxin 1) has a crucial role in the maintenance of lipophagic flux in macrophages. PRDX1 is more highly expressed than other anti-oxidant enzymes in monocytes and macrophages. We determined that Prdx1 deficiency induced excessive oxidative stress and impaired maintenance of autophagic flux in macrophages...
June 12, 2017: Autophagy
https://www.readbyqxmd.com/read/28602913/trpv4-calcium-permeable-channel-is-a-novel-regulator-of-oxidized-ldl-induced-macrophage-foam-cell-formation
#16
Rishov Goswami, Michael Merth, Shweta Sharma, Mazen O Alharbi, Helim Aranda-Espinoza, Xiaoping Zhu, Shaik O Rahaman
Cardiovascular disease is the number one cause of death in United States, and atherosclerosis, a chronic inflammatory arterial disease, is the most dominant underlying pathology. Macrophages are thought to orchestrate atherosclerosis by generating lipid-laden foam cells and by secreting inflammatory mediators. Emerging data support a role for a mechanical factor, e.g., matrix stiffness, in regulation of macrophage function, vascular elasticity, and atherogenesis. However, the identity of the plasma membrane mechanosensor and the mechanisms by which pro-atherogenic signals are transduced/maintained are unknown...
June 8, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28600950/histamine-promotes-the-differentiation-of-macrophages-from-cd11b-myeloid-cells-and-formation-of-foam-cells-through-a-stat6-dependent-pathway
#17
Lili Xu, Dengfeng Cheng, Zheyong Huang, Suling Ding, Weiwei Zhang, Hui Tan, Hongcheng Shi, Ruizhen Chen, Yunzeng Zou, Timothy C Wang, Xiangdong Yang, Junbo Ge
BACKGROUND AND AIMS: The enzyme histidine decarboxylase (Hdc), which generates histamine, is highly expressed in CD11b(+)Gr-1(+) myeloid cells that play a critical role in infection, inflammation and tumorigenesis. The aim of this study was to explore the role of Hdc-expressing CD11b(+) myeloid cells or histamine in atherogenesis. METHODS: Hdc-EGFP bacterial artificial chromosome (BAC) transgenic reporter mice (Hdc-EGFP) were used to track Hdc expression during the development of atherosclerosis...
May 23, 2017: Atherosclerosis
https://www.readbyqxmd.com/read/28596542/leukocyte-bim-deficiency-does-not-impact-atherogenesis-in-ldlr-mice-despite-a-pronounced-induction-of-autoimmune-inflammation
#18
Lieve Temmerman, Marijke M Westra, Ilze Bot, Bart J M van Vlijmen, Niek Van Bree, Martine Bot, Kim L L Habets, Tom G H Keulers, Johan van der Vlag, Thomas G Cotter, Theo J C van Berkel, Erik A L Biessen
Proapoptotic Bcl-2 family member Bim is particularly relevant for deletion of autoreactive and activated T and B cells, implicating Bim in autoimmunity. As atherosclerosis is a chronic inflammatory process with features of autoimmune disease, we investigated the impact of hematopoietic Bim deficiency on plaque formation and parameters of plaque stability. Bim (-/-) or wild type bone marrow transplanted ldlr (-/-) mice were fed a Western type diet (WTD) for 5 or 10 weeks, after which they were immunophenotyped and atherosclerotic lesions were analyzed...
June 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28592707/endothelial-nitric-oxide-synthase-independent-pleiotropic-effects-of-pitavastatin-against-atherogenesis-and-limb-ischemia-in-mice
#19
Takeshi Mitsuhashi, Ryoko Uemoto, Kazue Ishikawa, Sumiko Yoshida, Yasumasa Ikeda, Shusuke Yagi, Toshio Matsumoto, Masashi Akaike, Ken-Ichi Aihara
AIM: Statins have a protective impact against cardiovascular diseases through not only lipid-lowering effects but also pleiotropic effects, including activation of the endothelial nitric oxide synthase (eNOS) system. We aimed to clarify the protective effects of a statin against atherogenesis and ischemia in eNOS(-/-) mice. METHODS: Study 1. eNOS(-/-) Apolipoprotein E (ApoE)(-/-) mice were treated with a vehicle or pitavastatin (0.3 mg/kg/day) for 4 weeks...
June 6, 2017: Journal of Atherosclerosis and Thrombosis
https://www.readbyqxmd.com/read/28502908/chronic-administration-of-antioxidant-resin-from-virola-oleifera-attenuates-atherogenesis-in-ldlr-mice
#20
Paola Nogueira Coutinho, Beatriz Peters Pereira, Ana Claudia Hertel Pereira, Marcella Leite Porto, Arícia Leone Evangelista Monteiro de Assis, Afrânio Côgo Destefani, Silvana Santos Meyrelles, Elisardo Corral Vasquez, Breno Valentim Nogueira, Tadeu Uggere de Andrade, Denise Coutinho Endringer, Marcio Fronza, Thiago Melo Costa Pereira
ETHNOPHARMACOLOGICAL RELEVANCE: Virola oleifera (Schott) A. C. Smith, Myristicaceae has been largely used in traditional folk medicine in Brazil as an anti-inflammatory agent and our previous data indicated the antioxidant properties in other oxidative stress-related models. However, its effects on atherosclerosis (AT) are not yet investigated. AIMS OF THE STUDY: To evaluate the influence of resin from Virola oleifera (RV) on progression of AT in LDLr(-/-) mice...
July 12, 2017: Journal of Ethnopharmacology
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