scholarly journals Scavenger receptors: a key player in cardiovascular diseases

2012 ◽  
Vol 3 (4) ◽  
pp. 371-380 ◽  
Author(s):  
Mohammad Z. Ashraf ◽  
Anita Sahu
Keyword(s):  
Cardiovascular Diseases ◽  
Apoptotic Cell ◽  
Low Density Lipoprotein ◽  
Scavenger Receptor ◽  
Density Lipoprotein ◽  
Vascular Lesions ◽  
Great Promise ◽  
Term Therapy ◽  
Membrane Glycoproteins ◽  
The Individual

AbstractThe scavenger receptor (SR) super family consists of integral membrane glycoproteins that are involved in recognition of polyanionic structures of either endogenous (e.g., oxidized low-density lipoprotein) or exogenous (e.g., bacterial lipopolysaccharides) origin. SRs are structurally diverse and can be classified into seven different classes (A–G) based on the multidomain structure of the individual members. SRs are present on various types of tissues, such as vascular, adipose, and steroidogenic tissues. In addition to modified lipoprotein uptake, these proteins are also known to regulate apoptotic cell clearance, initiate signal transduction, and serve as pattern recognition receptors for pathogens. Different SRs are involved in many physiological and pathological processes; more importantly, the function of SRs is highly implicated in the initiation and progression of atherosclerotic plaque. Targeting the SR gene products that mediate the response to and uptake of modified lipids holds great promise in the prevention of cardiovascular diseases. Inhibition of SR expression using a combined gene therapy and RNA interference strategy also appears to be an option for long-term therapy. The present review focuses on the involvement of SRs in atherosclerosis, thrombosis, and other cardiovascular diseases. Moreover, the role of SRs is not restricted to vascular lesions; it is also implicated in a number of different cellular functions.

scholarly journals Lipoprotein Glomerulopathy-Like Lesions in Atherosclerotic Mice Defected With HDL Receptor SR-B1

2021 ◽  
Vol 8 ◽  
Author(s):  
Jiawei Liao ◽  
Jie Bai ◽  
Xiangbo An ◽  
Yang Liu ◽  
Yuhui Wang ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Low Density Lipoprotein ◽  
Scavenger Receptor ◽  
Density Lipoprotein ◽  
Chow Diet ◽  
Loss Of Function ◽  
Lipoprotein Glomerulopathy ◽  
Class B ◽  
Density Lipoprotein Receptor ◽  
Accelerate Atherosclerosis

High-density lipoprotein (HDL) homeostasis is important in maintaining both cardiovascular and renal health. Scavenger receptor class B type 1 (SR-B1), the major HDL receptor in mammals, plays a crucial role in reverse cholesterol transport and HDL metabolism. Evidence from mouse study has well demonstrated that HDL disorders caused by Srb1 inactivation accelerate atherosclerosis and even induce lethal cardiovascular diseases. However, the renal consequences of Srb1 dysfunction are still unknown. Here we explored this issue in both Srb1 knockout (Srb1-/-) mice and atherosclerotic low-density lipoprotein receptor knockout (Ldlr-/-) mice with Srb1 deletion. Our data showed that no apparent renal damage was observed in 5-month-old Srb1-/- mice fed on standard rodent chow diet as well as Srb1-/- mice fed on a high-fat diet (HFD) for 12 weeks. However, 5-month-old Srb1/Ldlr-/- mice fed on rodent chow had increased urinary albumin excretion and developed spontaneous intraglomerular Oil-red O (ORO)-positive lipoprotein deposition that is similar to lesions observed in human lipoprotein glomerulopathy (LPG). HFD feeding accelerated LPG-like lesions in Srb1/Ldlr-/- mice, inducing severe proteinuria and significantly promoting intraglomerular ORO-positive lipoprotein deposition. Interestingly, probucol reversed HFD-induced HDL disorders and almost fully abrogated LPG-like lesions in Srb1/Ldlr-/- mice. In conclusion, the present study demonstrates that SR-B1 dysfunction leads to LPG-like lesions in atherosclerotic mice, which could be rescued by probucol. SR-B1 loss-of-function mutant carriers therefore might be susceptible to developing metabolic nephropathy in addition to cardiovascular diseases, and probucol might be a potential therapeutics.

Risk predictors of arterial hypertension development in population of Mountain Shoriya of various ethnical origins

2019 ◽  
Vol 1 (3) ◽  
pp. 39-42
Author(s):  
T. A. Mulerova ◽  
M. Yu. Ogarkov ◽  
O. L. Barbarash
Keyword(s):  
Cardiovascular Diseases ◽  
Total Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoprotein Cholesterol ◽  
Type Settlement ◽  
The Family ◽  
Genotype C ◽  
Hypertension Development ◽  
Risk Predictors

1409 people (901 Shors, 508 non-indigenous people) from remote villages of Mountain Shoriya (Orton and Ust-Kabyrsa) and urban-type settlement Sheregesh took part in the survey. In Shors, the risk of developing hypertension was determined by elevated levels of total cholesterol and low density lipoprotein cholesterol, violation of carbohydrate metabolism, obesity, including its abdominal type, the family anamnesis of early cardiovascular diseases, and a carriage of prognostically unfavorable genotypes D/D and C/C of the corresponding genes ACE and AGTR 1 candidates; in the cohort of non-indigenous ethnos-elevated levels of total cholesterol and triglycerides, obesity, abdominal obesity, the family anamnesis of early cardiovascular diseases, a carrier of the minor genotype C/C of the AGTR 1 gene

scholarly journals The Effect of Helicobacter pylori Eradication on Lipid Levels: A Meta-Analysis

2021 ◽  
Vol 10 (5) ◽  
pp. 904
Author(s):  
Jun Watanabe ◽  
Masato Hamasaki ◽  
Kazuhiko Kotani
Keyword(s):  
Helicobacter Pylori ◽  
Cardiovascular Diseases ◽  
Meta Analysis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Levels ◽  
Pubmed Database ◽  
H Pylori ◽  
Meta Analyses

Introduction: Helicobacter pylori (H. pylori) infection is positively associated with cardiovascular diseases, but the involvement of lipids in this association remains unclear. The present study reviewed the changes in circulating lipid levels following H. pylori eradication. Methods: A PubMed database was searched until December 2020 to identify randomized control trials (RCTs) and non-RCTs investigating the effect of H. pylori eradication on the lipid levels in inverse variance-weighted, random-effects meta-analyses. Results: A total of 24 studies (four RCTs and 20 non-RCTs) with 5270 participants were identified. The post-eradication levels were increased for high-density lipoprotein cholesterol (HDL-C; mean difference (MD) 2.28 mg/dL, 95% confidence interval (CI) 1.90 to 2.66) and triglyceride (TG; MD 3.22 mg/dL, 95% CI 1.13 to 5.31) compared with the pre-eradication levels. H. pylori eradication resulted in little to no difference in the low-density lipoprotein-cholesterol levels (MD −2.33 mg/dL, 95% CI −4.92 to 0.26). In the analyses of RCTs only, the findings for elevated HDL-C levels, but not TG, were robust. Conclusions: H. pylori eradication increases the HDL-C levels. Further studies are needed to elucidate the effects of lipid changes following H. pylori eradication on cardiovascular diseases.

scholarly journals Platelet CD36 signaling through ERK5 promotes caspase-dependent procoagulant activity and fibrin deposition in vivo

2018 ◽  
Vol 2 (21) ◽  
pp. 2848-2861 ◽  
Author(s):  
Moua Yang ◽  
Andaleb Kholmukhamedov ◽  
Marie L. Schulte ◽  
Brian C. Cooley ◽  
Na’il O. Scoggins ◽  
...  
Keyword(s):  
Platelet Reactivity ◽  
Low Density Lipoprotein ◽  
Scavenger Receptor ◽  
Density Lipoprotein ◽  
Signaling Molecules ◽  
Chow Diet ◽  
Glycoprotein Vi ◽  
Platelet Signaling ◽  
Clinically Significant

Abstract Dyslipidemia is a risk factor for clinically significant thrombotic events. In this condition, scavenger receptor CD36 potentiates platelet reactivity through recognition of circulating oxidized lipids. CD36 promotes thrombosis by activating redox-sensitive signaling molecules, such as the MAPK extracellular signal-regulated kinase 5 (ERK5). However, the events downstream of platelet ERK5 are not clear. In this study, we report that oxidized low-density lipoprotein (oxLDL) promotes exposure of procoagulant phosphatidylserine (PSer) on platelet surfaces. Studies using pharmacologic inhibitors indicate that oxLDL-CD36 interaction–induced PSer exposure requires apoptotic caspases in addition to the downstream CD36-signaling molecules Src kinases, hydrogen peroxide, and ERK5. Caspases promote PSer exposure and, subsequently, recruitment of the prothrombinase complex, resulting in the generation of fibrin from the activation of thrombin. Caspase activity was observed when platelets were stimulated with oxLDL. This was prevented by inhibiting CD36 and ERK5. Furthermore, oxLDL potentiates convulxin/glycoprotein VI–mediated fibrin formation by platelets, which was prevented when CD36, ERK5, and caspases were inhibited. Using 2 in vivo arterial thrombosis models in apoE-null hyperlipidemic mice demonstrated enhanced arterial fibrin accumulation upon vessel injury. Importantly, absence of ERK5 in platelets or mice lacking CD36 displayed decreased fibrin accumulation in high-fat diet–fed conditions comparable to that seen in chow diet–fed animals. These findings suggest that platelet signaling through CD36 and ERK5 induces a procoagulant phenotype in the hyperlipidemic environment by enhancing caspase-mediated PSer exposure.

scholarly journals Identification of 31 novel mutations in the F8 gene in Spanish hemophilia A patients: structural analysis of 20 missense mutations suggests new intermolecular binding sites

Blood ◽  
2008 ◽  
Vol 111 (7) ◽  
pp. 3468-3478 ◽  
Author(s):  
Adoración Venceslá ◽  
María Ángeles Corral-Rodríguez ◽  
Manel Baena ◽  
Mónica Cornet ◽  
Montserrat Domènech ◽  
...  
Keyword(s):  
Hemophilia A ◽  
Low Density Lipoprotein ◽  
Scavenger Receptor ◽  
Density Lipoprotein ◽  
Missense Mutations ◽  
Factor X ◽  
Novel Mutations ◽  
Large Deletions ◽  
Function Relationship ◽  
The Impact

Abstract Hemophilia A (HA) is an X-linked bleeding disorder caused by a wide variety of mutations in the factor 8 (F8) gene, leading to absent or deficient factor VIII (FVIII). We analyzed the F8 gene of 267 unrelated Spanish patients with HA. After excluding patients with the common intron-1 and intron-22 inversions and large deletions, we detected 137 individuals with small mutations, 31 of which had not been reported previously. Eleven of these were nonsense, frameshift, and splicing mutations, whereas 20 were missense changes. We assessed the impact of the 20 substitutions based on currently available information about FV and FVIII structure and function relationship, including previously reported results of replacements at these and topologically equivalent positions. Although most changes are likely to cause gross structural perturbations and concomitant cofactor instability, p.Ala375Ser is predicted to affect cofactor activation. Finally, 3 further mutations (p.Pro64Arg, p.Gly494Val, and p.Asp2267Gly) appear to affect cofactor interactions with its carrier protein, von Willebrand factor, with the scavenger receptor low-density lipoprotein receptor–related protein (LRP), and/or with the substrate of the FVIIIapi•FIXa (Xase) complex, factor X. Characterization of these novel mutations is important for adequate genetic counseling in HA families, but also contributes to a better understanding of FVIII structure-function relationship.

Oxidized low-density lipoprotein as a biomarker of cardiovascular diseases

2014 ◽  
Vol 52 (2) ◽  
pp. 70-85 ◽  
Author(s):  
Andreja Trpkovic ◽  
Ivana Resanovic ◽  
Julijana Stanimirovic ◽  
Djordje Radak ◽  
Shaker A. Mousa ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein

scholarly journals CXCL16 Is Expressed in Podocytes and Acts as a Scavenger Receptor for Oxidized Low-Density Lipoprotein

2009 ◽  
Vol 174 (6) ◽  
pp. 2061-2072 ◽  
Author(s):  
Paul Gutwein ◽  
Mohamed Sadek Abdel-Bakky ◽  
Anja Schramme ◽  
Kai Doberstein ◽  
Nicole Kämpfer-Kolb ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Scavenger Receptor ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein

Abstract P249: Effects of Lifestyle Changes on Metabolism and Early Vascular Lesion in Healthy People

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Xu Fengcheng ◽  
Yu Chaoping ◽  
Liu Tianhu
Keyword(s):  
Healthy Lifestyle ◽  
Low Density Lipoprotein ◽  
Fasting Blood Glucose ◽  
Ankle Brachial Index ◽  
Density Lipoprotein ◽  
Vascular Lesion ◽  
Lifestyle Changes ◽  
Healthy People ◽  
Vascular Lesions ◽  
Before And After

Objective: Through propaganda and education on lifestyle change, we study the effects on metabolism and vascular lesions in healthy people. Methods: the healthy subjects that conform to the requirements, through propaganda and education on vascular health, through moderate exercise, proper control of starchy foods, low salt, low fat diet, reduce smoking and other lifestyle changes, compare changes in weight, renal function, fasting blood glucose, blood lipids and ankle brachial index (ABI), cardio ankle vascular index(CAVI) before and after lifestyle changes. Results: After lifestyle changed, the subjects’ body mass index [(23.13±3.18)kg/m 2 vs (22.67±3.36)kg/m 2 ], ABI[1.11±0.08 vs 1.09±0.09], CAVI[(7.14±1.13 ) vs (7. 01±1.18) ], serum creatinine[(84.31±22.41)umol/L vs (79.92±23.64)umol/L], blood uric acid[(337.79±102.17 )umol/L vs (328.12±88.33)umol/L], low density lipoprotein cholesterol[(2.49±0.65) mmol/L vs (2.37±0.69) mmol/L],all have good changes. Conclusion: Healthy lifestyle is good for metabolism and early vascular lesions, can improve metabolic disorder and slow the occurrence of arteriosclerosis.

scholarly journals Application of a New Processing Method to Post-LDL-apheresis Data

2002 ◽  
Vol 4 (3) ◽  
pp. 191-196 ◽  
Author(s):  
Franco Corsini ◽  
Arrigo F. G. Cicero ◽  
Antonia Giannuzzi ◽  
Antonio Gaddi
Keyword(s):  
Relative Error ◽  
Single Case ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Direct Consequence ◽  
Ldl Apheresis ◽  
Theoretical Function ◽  
New Processing ◽  
The Individual ◽  
Estimate Standard Error

Our aim was to elaborate a method to optimise treatment intervals for the individual low-density lipoprotein (LDL)-apheresis treated patients. After each treatment, plasma LDL concentrations show a time-related increase with a decreasing speed until a maximum level.We searched to interpret the post-LDL-apheresis experimental data trend as the physical process that produces the observed curve, so that the fitting presupposed theoretical function is a direct consequence of the physic process, because to establish the better time. Applying the proposed fitting method to a succession of 15 samples obtained from the mean of six plasmapheresis executed on five different subjects, small estimate standard error (5 mg/dl) and relative error (1.7%) with a dispersion evidently related to the experimental error were observed. Obviously, applying the same method to a single case, the dispersion is more marked (relative error <5%), with a SE of 10-13 mg/dl, even though the aspect of a casual phenomenon is conserved. Our physical interpretation appears to be a practical model to predict the LDL-rebound kinetic of the single patient.

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