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https://www.readbyqxmd.com/read/28534160/micrornas-new-therapeutic-targets-for-familial-hypercholesterolemia
#1
REVIEW
Amir Abbas Momtazi, Maciej Banach, Matteo Pirro, Evan A Stein, Amirhossein Sahebkar
Familial hypercholesterolemia (FH) is the most common inherited form of dyslipidemia and a major cause of premature cardiovascular disease. Management of FH mainly relies on the efficiency of treatments that reduce plasma low-density lipoprotein (LDL) cholesterol (LDL-C) concentrations. MicroRNAs (miRs) have been suggested as emerging regulators of plasma LDL-C concentrations. Notably, there is evidence showing that miRs can regulate the post-transcriptional expression of genes involved in the pathogenesis of FH, including LDLR, APOB, PCSK9, and LDLRAP1...
May 22, 2017: Clinical Reviews in Allergy & Immunology
https://www.readbyqxmd.com/read/28533932/metabolic-parameters-and-responsiveness-of-isolated-iliac-artery-in-ldlr-mice-role-of-aerobic-exercise-training
#2
Nádia F Garcia, Amanda Cs Sponton, Maria A Delbin, Juliana M Parente, Michele M Castro, Angelina Zanesco, Camila de Moraes
Physical inactivity and dyslipidemia are considered risk factors for cardiovascular diseases. There are few studies evaluating the effects of physical exercise in small-caliber artery in a model that mimics familial hypercholesterolemia. The aim of this study was to examine the effect of exercise training, at moderate intensity, on metabolic parameters and iliac artery responsiveness in LDL(-/-) mice. Sedentary (SD) and trained (TR) mice performed AET (5 days/week, 60 minutes/day at 60-70% of maximum speed) during 8 weeks...
2017: American Journal of Cardiovascular Disease
https://www.readbyqxmd.com/read/28529649/sak-hv-triggered-a-short-period-lipid-lowering-biotherapy-based-on-the-energy-model-of-liver-proliferation-via-a-novel-pathway
#3
Chao Zhang, Zhiguang Huang, Haoran Jing, Wenliang Fu, Min Yuan, Wenrong Xia, Ling Cai, Xiangdong Gan, Yao Chen, Minji Zou, Minhui Long, Jiaxi Wang, Min Wang, Donggang Xu
The accumulations of excess lipids within liver and serum are defined as non-alcoholic fatty liver disease (NAFLD) and hyperlipemia respectively. Both of them are components of metabolic syndrome that greatly threaten human health. Here, a recombinant fusion protein (SAK-HV) effectively treated NAFLD and hyperlipemia in high-fat-fed ApoE(-/-) mice, quails and rats within just 14 days. Its triglyceride and cholesterol-lowering effects were significantly better than that of atorvastatin during the observation period...
2017: Theranostics
https://www.readbyqxmd.com/read/28527015/a-genome-wide-association-study-identifies-the-genomic-region-associated-with-shell-color-in-yesso-scallop-patinopecten-yessoensis
#4
Liang Zhao, Yangping Li, Yajuan Li, Jiachen Yu, Huan Liao, Shuyue Wang, Jia Lv, Jun Liang, Xiaoting Huang, Zhenmin Bao
The shell color polymorphism widely exists in economic shellfish, which not only results in a better visual perception but also shows great value as an economic trait for breeding. Small numbers of reddish-orange shell Yesso scallops, Patinopecten yessoensis, were found in cultured populations compared to the brown majority. In this study, a genome-wide association study was conducted to understand the genetic basis of shell color. Sixty-six 2b-RAD libraries with equal numbers of reddish-orange and brown shell individuals were constructed and sequenced using the Illumina HiSeq 2000 platform...
May 19, 2017: Marine Biotechnology
https://www.readbyqxmd.com/read/28526856/2-hydroxypropyl-beta-cyclodextrin-hp%C3%AE-cd-reduces-age-related-lipofuscin-accumulation-through-a-cholesterol-associated-pathway
#5
Jason Gaspar, Jacques Mathieu, Pedro Alvarez
Oxidative stress causes significant increases in both cholesterol uptake and intracellular accumulation of the aging biomarker lipofuscin. Here we show that HPβCD addition mitigates these adverse effects in human fibroblasts by significantly reducing LDLr and SREBP1 gene expression. In the absence of oxidative stress, HPβCD addition induces a paradoxical response, increasing cholesterol accumulation (but not lipofuscin) via upregulation of cholesterol biosynthesis. These two distinct, but opposite effects highlight a previously overlooked therapeutic consideration: the cholesterol content of the treated cell determines which cholesterol pathways, either beneficial or harmful, are responsive to HPβCD...
May 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28526391/withdrawal-from-high-carbohydrate-high-saturated-fat-diet-changes-saturated-fat-distribution-and-improves-hepatic-low-density-lipoprotein-receptor-expression-to-ameliorate-metabolic-syndrome-in-rats
#6
Ankita Hazarika, Himadri Kalita, Mohan Chandra Kalita, Rajlakshmi Devi
OBJECTIVE: The "lipid hypothesis" determined that saturated fatty acid (SFA) raises low-density lipoprotein cholesterol, thereby increasing the risk for metabolic syndrome (MetS). The aim of this study was to investigate the effect of subchronic withdrawal from a high-carbohydrate, high-saturated fat (HCHF) diet during MetS with reference to changes in deleterious SFA (C12:0, lauric acid; C14:0, myristic acid; C16:0, palmitic acid; C18:0, stearic acid) distribution in liver, white adipose tissue (WAT), and feces...
June 2017: Nutrition
https://www.readbyqxmd.com/read/28522295/reversal-of-adipose-tissue-loss-by-probucol-in-mice-with-deficiency-of-both-scavenger-receptor-class-b-type-1-and-ldl-receptor-on-high-fat-diet
#7
Xin Guo, Jiawei Liao, Xiaomin Huang, Yuhui Wang, Wei Huang, George Liu
Scavenger receptor class B type 1(SR-B1) and low density lipoprotein receptor (LDLR) play vital roles in cholesterol homeostasis. Previous studies indicated a strong link between cholesterol and adipose tissue (AT). In this study, adult male SR-B1 and LDLR double knockout (DKO) mice were fed with high fat diet (HFD) for 3 months. Interestingly, we found severe loss of AT in DKO mice fed with HFD. To reverse the AT loss in DKO mice, 1% probucol was added in HFD. In DKO mice on HFD, plasma total cholesterol (TC) and free cholesterol (FC) levels were increased 6 and 15 folds respectively compared with wild type (WT) mice...
May 15, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28521874/sirna-mediated-inhibition-of-srebp-cleavage-activating-protein-reduces-dyslipidemia-in-spontaneously-dysmetabolic-rhesus-monkeys
#8
Beth Ann Murphy, Marija Tadin-Strapps, Kristian Jensen, Robin Mogg, Andy Liaw, Kithsiri Herath, Gowri Bhat, David G McLaren, Stephen F Previs, Shirly Pinto
BACKGROUND: SREBP cleavage-activating protein (SCAP) is a cholesterol binding endoplasmic reticulum (ER) membrane protein that is required to activate SREBP transcription factors. SREBPs regulate genes involved in lipid biosynthesis. They also influence lipid clearance by modulating the expression of LDL receptor (LDLR) and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. Inhibiting SCAP decreases circulating PCSK9, triglycerides (TG), and LDL-cholesterol (LDL-C), both in vitro and in vivo...
June 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28515357/e2f1-inhibits-circulating-cholesterol-clearance-by-regulating-pcsk9-expression-in-the-liver
#9
Qiuwen Lai, Albert Giralt, Cédric Le May, Lianjun Zhang, Bertrand Cariou, Pierre-Damien Denechaud, Lluis Fajas
Cholesterol accumulation in the liver is an early event in nonalcoholic fatty liver disease (NAFLD). Here, we demonstrate that E2F1 plays a crucial role in maintaining cellular cholesterol homeostasis by regulating cholesterol uptake via proprotein convertase subtilisin/kexin 9 (PCSK9), an enzyme that promotes low-density lipoprotein receptor (LDLR) degradation upon activation. E2f1-/- mice display reduced total plasma cholesterol levels and increased cholesterol content in the liver. In this study, we show that E2f1 deletion in cellular and mouse models leads to a marked decrease in Pcsk9 expression and an increase in LDLR expression...
May 18, 2017: JCI Insight
https://www.readbyqxmd.com/read/28513806/increased-activity-of-vascular-adenosine-deaminase-in-atherosclerosis-and-therapeutic-potential-of-its-inhibition
#10
Barbara Kutryb-Zajac, Lukasz Mateuszuk, Paulina Zukowska, Agnieszka Jasztal, Magdalena A Zabielska, Marta Toczek, Patrycja Jablonska, Agnieszka Zakrzewska, Barbara Sitek, Jan Rogowski, Romuald Lango, Ewa M Slominska, Stefan Chlopicki, Ryszard T Smolenski
Aims: Extracellular nucleotides and adenosine that are formed or degraded by membrane-bound ecto-enzymes could affect atherosclerosis by regulating the inflammation and thrombosis. This study aimed to evaluate a relation between ecto-enzymes that convert extracellular adenosine triphosphate to adenine dinucleotide phosphate, adenosine monophosphate, adenosine, and inosine on the surface of the vessel wall with the severity or progression of experimental and clinical atherosclerosis. Furthermore, we tested whether the inhibition of adenosine deaminase will block the development of experimental atherosclerosis...
November 1, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/28511572/mtor-drives-cerebral-blood-flow-and-memory-deficits-in-ldlr-mice-modeling-atherosclerosis-and-vascular-cognitive-impairment
#11
Jordan B Jahrling, Ai-Ling Lin, Nicholas DeRosa, Stacy A Hussong, Candice E Van Skike, Milena Girotti, Martin Javors, Qingwei Zhao, Leigh Ann Maslin, Reto Asmis, Veronica Galvan
We recently showed that mTOR attenuation blocks progression and abrogates established cognitive deficits in Alzheimer's disease (AD) mouse models. These outcomes were associated with the restoration of cerebral blood flow (CBF) and brain vascular density (BVD) resulting from relief of mTOR inhibition of NO release. Recent reports suggested a role of mTOR in atherosclerosis. Because mTOR drives aging and vascular dysfunction is a universal feature of aging, we hypothesized that mTOR may contribute to brain vascular and cognitive dysfunction associated with atherosclerosis...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28506388/discordant-response-of-low-density-lipoprotein-cholesterol-and-lipoprotein-a-levels-to-monoclonal-antibodies-targeting-proprotein-convertase-subtilisin-kexin-type-9
#12
Jonathan B Edmiston, Nathan Brooks, Hagai Tavori, Jessica Minnier, Bart Duell, Jonathan Q Purnell, Tina Kaufman, Cezary Wojcik, Szilard Voros, Sergio Fazio, Michael D Shapiro
BACKGROUND: Clinical trials testing proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) have demonstrated an unanticipated but significant lipoprotein (a) (Lp(a))-lowering effect, on the order of 25% to 30%. Although the 50% to 60% reduction in low-density lipoprotein (LDL)-cholesterol (LDL-C) achieved by PCSK9i is mediated through its effect on LDL receptor (LDLR) preservation, the mechanism for Lp(a) lowering is unknown. OBJECTIVE: We sought to characterize the degree of concordance between LDL-C and Lp(a) lowering because of PCSK9i in a standard of care patient cohort...
May 2017: Journal of Clinical Lipidology
https://www.readbyqxmd.com/read/28504688/accelerated-atherosclerosis-development-in-c57bl6-mice-by-overexpressing-aav-mediated-pcsk9-and-partial-carotid-ligation
#13
Sandeep Kumar, Dong-Won Kang, Amir Rezvan, Hanjoong Jo
Studying the role of a particular gene in atherosclerosis typically requires a time-consuming and often difficult process of generating double knockouts or transgenics on ApoE(-/-) or LDL receptor (LDLR)(-/-) background. Recently, it was reported that adeno-associated-virus-8 (AAV8)-mediated overexpression of PCSK9 (AAV8-PCSK9) rapidly induced hyperlipidemia. However, using this method in C57BL6 wild-type (C57) mice, it took ~3 months to develop atherosclerosis. Our partial carotid ligation model is used to rapidly develop atherosclerosis by inducing disturbed flow in the left common carotid artery within 2 weeks in ApoE(-/-) or LDLR(-/-) mice...
May 15, 2017: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/28502908/chronic-administration-of-antioxidant-resin-from-virola-oleifera-attenuates-atherogenesis-in-ldlr-mice
#14
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...
May 11, 2017: Journal of Ethnopharmacology
https://www.readbyqxmd.com/read/28502508/plasma-lipoprotein-a-levels-in-patients-with-homozygous-autosomal-dominant-hypercholesterolemia
#15
Barbara Sjouke, Reyhana Yahya, Michael W T Tanck, Joep C Defesche, Jacqueline de Graaf, Albert Wiegman, John J P Kastelein, Monique T Mulder, G Kees Hovingh, Jeanine E Roeters van Lennep
BACKGROUND: Patients with autosomal dominant hypercholesterolemia (ADH), caused by mutations in either low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), or proprotein convertase subtilisin-kexin type 9 (PCSK9) are characterized by high low-density lipoprotein cholesterol levels and in some studies also high lipoprotein(a) (Lp(a)) levels were observed. The question remains whether this effect on Lp(a) levels is gene-dose-dependent in individuals with either 0, 1, or 2 LDLR or APOB mutations...
March 2017: Journal of Clinical Lipidology
https://www.readbyqxmd.com/read/28500865/dihydromyricetin-ameliorates-atherosclerosis-in-ldl-receptor-deficient-mice
#16
Ting Ting Liu, Yi Zeng, Kun Tang, XueMeng Chen, Wei Zhang, Xiao Le Xu
BACKGROUND AND AIMS: Dihydromyricetin, the most abundant flavonoid in Ampelopsis grossedentata, exerts numerous pharmacological activities, including anti-inflammatory, antioxidant, hepatoprotective, and lipid regulatory activities; however, its protective effect against atherosclerosis remains poorly understood. The aim of the present study was to evaluate the effects of dihydromyricetin on high fat diet (HFD)-induced atherosclerosis using LDL receptor deficient (LDLr(-/-)) mice. METHODS: Blood samples were collected for determination of serum lipid profiles, oxidized LDL (ox-LDL) and pro-inflammatory cytokines...
May 5, 2017: Atherosclerosis
https://www.readbyqxmd.com/read/28500604/a-primer-to-angiotensin-peptide-isolation-stability-and-analysis-by-nano-liquid-chromatography-with-mass-detection
#17
Mariola Olkowicz, Stefan Chlopicki, Ryszard T Smolenski
The renin-angiotensin system (RAS) is an important element of cardiovascular and renal physiology and targeting the RAS by renin inhibitors, angiotensin (Ang) converting enzyme (ACE) inhibitors and Ang II type 1 receptor antagonists is effective in the treatment of hypertension, heart failure, and atherosclerosis. Quantification of Ang peptides is critical to establish the status of the RAS, but it is challenging due to low Ang peptides concentrations (fmol/mL or fmol/g), abundance of interfering substances, post sampling conversions, and difficulties with the specificity of the assay...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28500602/a-new-mouse-model-for-introduction-of-aortic-aneurysm-by-implantation-of-deoxycorticosterone-acetate-pellets-or-aldosterone-infusion-in-the-presence-of-high-salt
#18
Shu Liu, Ming C Gong, Zhenheng Guo
Dysfunction of the renin-angiotensin-aldosterone system (RAAS) has been implicated in the etiologies of many cardiovascular diseases, including aortic aneurysm. In particular, the infusion of angiotensin II (Ang II) in the apolipoprotein E-deficient mice (apoE-/-) and low density lipoprotein receptor knockout mice (LDLR-/-) to induce aortic aneurysm has been extensively used in the field. In contrast, whether aldosterone (Aldo), an essential component of RAAS and a downstream effector of Ang II, is involved in aortic aneurysm is largely unknown...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28499924/hypercholesterolemia-causes-circadian-dysfunction-a-potential-risk-factor-for-cardiovascular-disease
#19
Makoto Akashi, Ritsuko Matsumura, Takahiro Matsuo, Yuki Kubo, Hiroshi Komoda, Koichi Node
Hypercholesterolemia is a well-known risk factor for a wide range of diseases in developed countries. Here, we report that mice lacking functional LDLR (low density lipoprotein receptor), an animal model of human familial hypercholesterolemia, show circadian abnormalities. In free running behavioral experiments in constant darkness, these mice showed a prolonged active phase and distinctly bimodal rhythms. Even when the circadian rhythms were entrained by light and dark cycles, these mice showed a significant attenuation of behavioral onset intensity at the start of the dark period...
April 27, 2017: EBioMedicine
https://www.readbyqxmd.com/read/28495363/app-aplp2-and-lrp1-interact-with-pcsk9-but-are-not-required-for-pcsk9-mediated-degradation-of-the-ldlr-in-vivo
#20
Ting Fu, YangYang Guan, Junjie Xu, Yan Wang
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secreted protein that post-transcriptionally regulates the levels of hepatic low-density lipoprotein receptors (LDLRs). PCSK9 binds to the extracellular domain of the LDLR, and the PCSK9-LDLR complex is internalized through canonical clathrin-dependent endocytosis and then delivered to lysosomes for degradation. The mechanism by which PCSK9 blocks recycling of the LDLR has not been fully defined. Previous reports showed that amyloid precursor-like protein 2 (APLP2) interacts with PCSK9, but its role in PCSK9-mediated LDLR degradation remains controversial...
May 8, 2017: Biochimica et Biophysica Acta
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