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| 1 | Inflammation, oxidative stress and renin angiotensin system in atherosclerosis显示文摘Atherosclerosis is a chronic inflammatory disease associated with cardiovascular dysfunction including myocardial infarction, unstable angina, sudden cardiac death, stroke and peripheral thromboses. It has been predicted that atherosclerosis will be the primary cause of death in the world by 2020. Atherogenesis is initiated by endothelial injury due to oxidative stress associated with cardiovascular risk factors including diabetes mellitus, hypertension, cigarette smoking, dyslipidemia, obesity, and metabolic syndrome. The impairment of the endothelium associated with cardiovascular risk factors creates an imbalance between vasodilating and vasoconstricting factors, in particular, an increase in angiotensin Ⅱ(Ang Ⅱ) and a decrease in nitric oxide. The renin-angiotensin system(RAS), and its primary mediator Ang Ⅱ, also have a direct influence on the progression of the atherosclerotic process via effects on endothelial function, inflammation, fibrinolytic balance, and plaque stability. Anti-inflammatory agents [statins, secretory phospholipase A2 inhibitor, lipoprotein-associated phospholipase A2 inhibitor, 5-lipoxygenase activating protein, chemokine motif ligand-2, C-C chemokine motif receptor 2 pathway inhibitors, methotrexate, IL-1 pathway inhibitor and RAS inhibitors(angiotensin-converting enzyme inhibitors)], Ang Ⅱ receptor blockers and ranin inhibitors may slow inflammatory processes and disease progression. Several studies in human using anti-inflammatory agents and RAS inhibitors revealed vascular benefits and reduced progression of coronary atherosclerosis in patients with stable angina pectoris; decreased vascular inflammatory markers, improved common carotid intima-media thickness and plaque volume in patients with diagnosed atherosclerosis. Recent preclinical studies have demonstrated therapeutic efficacy of vitamin D analogs paricalcitol in Apo E-deficient atherosclerotic mice. | Kazim Husain Wilfredo Hernandez Rais A Ansari Leon Ferder | 2015 | World Journal of Biological Chemistry2015，6，3： | 84 |
| 2 | 在心血管的疾病的先进 glycation 结束产品的角色显示文摘 Advanced glycation end products(AGEs) are produced through the non enzymatic glycation and oxidation of proteins,lipids and nucleic acids.Enhanced formation of AGEs occurs particularly in conditions associated with hyperglycaemia such as diabetes mellitus(DM).AGEs are believed to have a key role in the development and progression of cardiovascular disease in patients with DM through the modif ication of the structure,function and mechanical properties of tissues through crosslinking intracellular as well as extracellular matrix proteins and through modulating cellular processes through binding to cell surface receptors [receptor for AGEs(RAGE)].A number of studies have shown a correlation between serum AGE levels and the development and severity of heart failure(HF).Moreover,some studies have suggested that therapies targeted against AGEs may have therapeutic potential in patients with HF.The purpose of this review is to discuss the role of AGEs in cardiovascular disease and in particular in heart failure,focussing on both cellular mechanisms of action as well as highlighting how targeting AGEs may represent a novel therapeutic strategy in the treatment of HF. | Zeinab Hegab Stephen Gibbons Ludwig Neyses Mamas A Mamas | 2012 | World Journal of Cardiology2012，4，4： | 58 |
| 3 | Lipid homeostasis and the formation of macrophage-derived foam cells in atherosclerosis显示文摘Atherosclerosis is a chronic,inflammatory disorder characterized by the deposition of excess lipids in the arterial intima.The formation of macrophage-derived foam cells in a plaque is a hallmark of the development of atherosclerosis.Lipid homeostasis,especially cho-lesterol homeostasis,plays a crucial role during the formation of foam cells.Recently,lipid droplet-associated proteins,including PAT and CIDE family proteins,have been shown to control the development of athero-sclerosis by regulating the formation,growth,stabiliza-tion and functions of lipid droplets in macrophage-derived foam cells.This review focuses on the potential mechanisms of formation of macrophage-derived foam cells in atherosclerosis with particular emphasis on the role of lipid homeostasis and lipid droplet-associated proteins.Understanding the process of foam cell for-mation will aid in the future discovery of novel thera-peutic interventions for atherosclerosis. | Yuan Yuan Peng Li Jing Ye | 2012 | Protein & Cell2012，3，3： | 44 |
| 4 | Role of Helicobacter pylori infection in pathogenesis of atherosclerosis显示文摘Though a century old hypothesis, infection as a cause for atherosclerosis is still a debatable issue. Epidemiological and clinical studies had shown a possible association but inhomogeneity in the study population and study methods along with potential confounders have yielded conflicting results. Infection triggers a chronic inflammatory state which along with other mechanisms such as dyslipidemia, hyper-homocysteinemia, hypercoagulability, impaired glucose metabolism and endothelial dysfunction, contribute in pathogenesis of atherosclerosis. Studies have shown a positive relations between Cytotoxic associated gene-A positive strains of Helicobacter pylori and vascular diseases such as coronary artery disease and stroke. Infection mediated genetic modulation is a new emerging theory in this regard. Further large scale studies on infection and atherosclerosis focusing on multiple pathogenetic mechanisms may help in refining our knowledge in this aspect. | Rajesh Vijayvergiya Ramalingam Vadivelu | 2015 | World Journal of Cardiology2015，7，3： | 37 |
| 5 | Oxidative stress:New insights on the association of nonalcoholic fatty liver disease and atherosclerosis显示文摘Non-alcoholic fatty liver disease(NAFLD) represents the most common and emerging chronic liver disease worldwide. It includes a wide spectrum of liver diseasesranging from simple fatty liver to non-alcoholic steatohepatitis(NASH),which may progress to fibrosis and more severe liver complications such as cirrhosis,hepatocellular carcinoma and liver mortality. NAFLD is strongly associated with obesity,insulin resistance,hypertension,and dyslipidaemia,and is now regarded as the liver manifestation of the metabolic syndrome. The increased mortality of patients with NAFLD is primarily a result of cardiovascular disease and,to a lesser extent,to liver related diseases. Increased oxidative stress has been reported in both patients with NAFLD and patient with cardiovascular risk factors. Thus,oxidative stress represents a shared pathophysiological disorder between the two conditions. Several therapeutic strategies targeting oxidative stress reduction in patients with NAFLD have been proposed,with conflicting results. In particular,vitamin E supplementation has been suggested for the treatment of non-diabetic,non-cirrhotic adults with active NASH,although this recommendation is based only on the results of a single randomized controlled trial. Other antioxidant treatments suggested are resveratrol,silybin,L-carnitine and pentoxiphylline. No trial so far,has evaluated the cardiovascular effects of antioxidant treatment in patients with NAFLD. New,large-scale studies including as end-point also the assessment of the atherosclerosis markers are needed. | Licia Polimeni Maria Del Ben Francesco Baratta Ludovica Perri Fabiana Albanese Daniele Pastori Francesco Violi Francesco Angelico | 2015 | World Journal of Hepatology2015，7，10： | 23 |
| 6 | Epidemiology of age-related macular degeneration (AMD): associations with cardiovascular disease phenotypes and lipid factors显示文摘Age-related macular degeneration(AMD)is the leading cause of irreversible blindness in adults over 50 years old.Genetic,epidemiological,and molecular studies are beginning to unravel the intricate mechanisms underlying this complex disease,which implicate the lipid-cholesterol pathway in the pathophysiology of disease development and progression.Many of the genetic and environmental risk factors associated with AMD are also associated with other complex degenerative diseases of advanced age,including cardiovascular disease(CVD).In this review,we present epidemiological findings associating AMD with a variety of lipid pathway genes,cardiovascular phenotypes,and relevant environmental exposures.Despite a number of studies showing significant associations between AMD and these lipid/cardiovascular factors,results have been mixed and as such the relationships among these factors and AMD remain controversial.It is imperative that researchers not only tease out the various contributions of such factors to AMD development but also the connections between AMD and CVD to develop optimal precision medical care for aging adults. | Katie L.Pennington Margaret M.DeAngelis | 2016 | Eye and Vision2016，3，1： | 22 |
| 7 | Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis显示文摘Objective PERK/eI F2α/CHOP is a major signaling pathway mediating endoplasmic reticulum(ER) stress related with atherosclerosis.Oxidized LDL(ox-LDL) also induces endothelial apoptosis and plays a vital role in the initiation and progression of atherosclerosis.The present study was conducted to explore the regulatory effect of ox-LDL on PERK/e IF2α/CHOP signaling pathway in vascular endothelial cells.Methods The effects of ox-LDL on PERK and p-e IF2α protein expression of primary human umbilical vein endothelial cells(HUVECs) were investigated by Western blot analysis.PERK gene silencing and selective eI F2α phosphatase inhibitor,salubrinal were used to inhibit the process of ox-LDL induced endothelial cell apoptosis,caspase-3 activity,and CHOP mR NA level.Results Ox-LDL treatment significantly increased the expression of PERK,PERK-mediated inactivation of e IF2α phosphorylation,and the expression of CHOP,as well as the caspase-3 activity and apoptosis.The effects of ox-LDL were markedly decreased by knocking down PERK with stable transduction of lentiviral sh RNA or by selective eI F2α phosphatase inhibitor,salubrinal.Conclusion This study provides the first evidence that ox-LDL induces apoptosis in vascular endothelial cells mediated largely via the PERK/eI F2α/CHOP ER-stress pathway.It adds new insights into the molecular mechanisms underlying the pathogenesis and progression of atherosclerosis. | TAO Yong Kang YU Pu Lin BAI Yong Ping YAN Sheng Tao ZHAO Shui Ping ZHANG Guo Qiang | 2016 | Biomedical and Environmental Sciences2016，29，12： | 21 |
| 8 | Animal models for the atherosclerosis research:a review显示文摘Atherosclerosis is a leading cause of death worldwide,and its mechanisms are still unclear.However,various animal models have significantly advanced our understanding of the mechanisms involved in atherosclerosis and have allowed the evaluation of therapeutic options.The aim of this paper is to review those animal models(i.e.,rabbits,mice,rats,guinea pigs,hamsters,avian,carnivores,swine,and,non-human primates)that have been used to study atherosclerosis.Though there is no single perfect animal model that completely replicates the stages of human atherosclerosis,cholesterol feeding and mechanical endothelial injury are two common features shared by most models of atherosclerosis.Further,with the development of genetically modified animals,these models are significantly broadening our understanding of the pathogenesis of atherosclerosis. | Xiangdong Li Yuanwu Liu Hua Zhang Liming Ren Qiuyan Li Ning Li | 2011 | Protein & Cell2011，2，3： | 21 |
| 9 | Inflammation and atherosclerosis: signaling pathways and therapeutic intervention显示文摘Atherosclerosis is a chronic inflammatory vascular disease driven by traditional and nontraditional risk factors.Genome-wide association combined with clonal lineage tracing and clinical trials have demonstrated that innate and adaptive immune responses can promote or quell atherosclerosis.Several signaling pathways,that are associated with the inflammatory response,have been implicated within atherosclerosis such as NLRP3 inflammasome,toll-like receptors,proprotein convertase subtilisin/kexin type 9. | Peng Kong Zi-Yang Cui Xiao-Fu Huang Dan-Dan Zhang Rui-Juan Guo Mei Han | 2022 | Signal Transduction and Targeted Therapy2022，7，5： | 20 |
| 10 | Dissecting the role of AMP-activated protein kinase in human diseases显示文摘AMP-activated protein kinase(AMPK), known as a sensor and a master of cellular energy balance, integrates various regulatory signals including anabolic and catabolic metabolic processes.Accompanying the application of genetic methods and a plethora of AMPK agonists, rapid progress has identified AMPK as an attractive therapeutic target for several human diseases, such as cancer, type2 diabetes, atherosclerosis, myocardial ischemia/reperfusion injury and neurodegenerative disease. The role of AMPK in metabolic and energetic modulation both at the intracellular and whole body levels has been reviewed elsewhere. In the present review, we summarize and update the paradoxical role of AMPK implicated in the diseases mentioned above and put forward the challenge encountered. Thus it will be expected to provide important clues for exploring rational methods of intervention in human diseases. | Jin Li Liping Zhong Fengzhong Wang Haibo Zhu | 2017 | Acta Pharmaceutica Sinica B2017，7，3： | 18 |
| 11 | Infectious burden and atherosclerosis: A clinical issue显示文摘Atherosclerotic cardiovascular diseases, chronic inflam-matory diseases of multifactorial etiology, are the lead-ing cause of death worldwide. In the last decade, more infectious agents, labeled as 'infectious burden', rather than any single pathogen, have been showed to con-tribute to the development of atherosclerosis through different mechanisms. Some microorganisms, such as Chlamydia pneumoniae(C. pneumoniae), human cytomegalovirus, etc. may act directly on the arterial wall contributing to endothelial dysfunction, foam cell formation, smooth muscle cell proliferation, platelet ag-gregation as well as cytokine, reactive oxygen specie, growth factor, and cellular adhesion molecule produc-tion. Others, such as Helicobacter pylori(H. pylori), in-fluenza virus, etc. may induce a systemic inflammation which in turn may damage the vascular wall(e.g., by cytokines and proteases). Moreover, another indirect mechanism by which some infectious agents(such as H. pylori, C. pneumoniae, periodontal pathogens, etc.) may play a role in the pathogenesis of atherosclero-sis is molecular mimicry. Given the complexity of the mechanisms by which each microorganism may con-tribute to atherosclerosis, defining the interplay of moreinfectious agents is far more difficult because the pro-atherogenic effect of each pathogen might be ampli-fied. Clearly, continued research and a greater aware-ness will be helpful to improve our knowledge on the complex interaction between the infectious burden and atherosclerosis. | Rosa Sessa Marisa Di Pietro Simone Filardo Ombretta Turriziani | 2014 | World Journal of Clinical Cases2014，2，7： | 17 |
| 12 | Novel concepts in radiation-induced cardiovascular disease显示文摘Radiation-induced cardiovascular disease(RICVD) is the most common nonmalignant cause of morbidity and mortality among cancer survivors who have undergone mediastinal radiation therapy(RT).Cardiovascular complications include effusive or constrictive pericarditis,cardiomyopathy,valvular heart disease,and coronary/vascular disease.These are pathophysiologically distinct disease entities whose prevalence varies depending on the timing and extent of radiation exposure to the heart and great vessels.Although refinements in RT dosimetry and shielding will inevitably limit future cases of RICVD,the increasing number of long-term cancer survivors,including those treated with older higher-dose RT regimens,will ensure a steady flow of afflicted patients for the foreseeable future.Thus,there is a pressing need for enhanced understanding of the disease mechanisms,and improved detection methods and treatment strategies.Newly characterized mechanisms responsible for the establishment of chronic fibrosis,such as oxidative stress,inflammation and epigenetic modifications,are discussed and linked to potential treatments currently under study.Novel imaging modalities may serve as powerful screening tools in RICVD,and recent research and expert opinion advocating their use is introduced.Data arguing for the aggressive use of percutaneous interventions,such as transcutaneous valve replacement and drug-eluting stents,are examined and considered in the context of prior therapeutic approaches.RICVD and its treatment options are the subject of a rich and dynamic body of research,and patients who are at risk or suffering from this disease will benefit from the care of physicians with specialty expertise in the emerging field of cardiooncology. | Jason R Cuomo Gyanendra K Sharma Preston D Conger Neal L Weintraub | 2016 | World Journal of Cardiology2016，8，9： | 17 |
| 13 | Mitochondrial dysfunction and mitochondrial DNA mutations in atherosclerotic complications in diabetes显示文摘Mitochondrial DNA(mtDNA) is particularly prone to oxidation due to the lack of histones and a deficient mismatch repair system.This explains an increased mutation rate of mtDNA that results in heteroplasmy,e.g.,the coexistence of the mutant and wild-type mtDNA molecules within the same mitochondrion.In diabetes mellitus,glycotoxicity,advanced oxidative stress,collagen cross-linking,and accumulation of lipid peroxides in foam macrophage cells and arterial wall cells may significantly decrease the mutation threshold required for mitochondrial dysfunction,which in turn further contributes to the oxidative damage of the diabetic vascular wall,endothelial dysfunc-tion,and atherosclerosis. | Dimitry A Chistiakov Igor A Sobenin Yuri V Bobryshev Alexander N Orekhov | 2012 | World Journal of Cardiology2012，4，5： | 17 |
| 14 | Chinese Yellow Wine Inhibit Production of Homocysteine-induced Extracellular Matrix Metalloproteinase-2 in Cultured Rat Vascular Smooth Muscle Cells显示文摘Objectives Regular consumption of moderate amounts of Chinese yellow wine is associated with a reduced risk of coronary disease. Matrix metalloproteinases (MMPs) that participate in extracellular matrix degradation have been involved in atherosclerotic plaque growth and instability. The present research aimed to study the effects of Chinese yellow wine on the production of homocysteine-induced extracellular MMP-2 in cultured rats' vascular smooth muscle cells. Methods The effects of different homocysteine levels (0-1000 ?滋mol/l) on MMP-2 production, and the effects of Chinese yellow wine with low alcohol concentrations (12-19%) on homocysteine-induced MMP-2 in cultured rat vascular smooth muscle cells (VSMCs) were examined using gelatin zymography and western blotting. The changes of MMP-2 under various treatments for 12 h, 24 h and 48 h were further compared. Results Homocysteine (50-1000 ?滋mol/l) increased the production of MMP-2 significantly in a dose-dependent manner. Increased production of MMP-2 induced by homocysteine was reduced by extracellularly added Chinese yellow wine. Production of MMP-2 under various treatments for 48 h increased more than 12 h and 24 h. Conclusions Extracellularly added Chinese yellow wine decreased homocysteine-induced MMP-2 secretion. The inhibitory effect of yellow wine on the activation of MMP-2 might contribute to their beneficial effects on the cardiovascular system. | 郭航远 邢杨波 彭放 杨彪 裘宇芳 游斌权 李刚 朱敏 袁敏 何益平 周妍 Lee Jong-Dae | 2007 | South China Journal of Cardiology2007，0，1： | 16 |
| 15 | Biological drug and drug delivery-mediated immunotherapy显示文摘The initiation and development of major infammatory diseases,i.e.,cancer,vascular infammation,and some autoimmune diseases are closely linked to the immune system.Biologics-based immunotherapy is exerting a critical role against these diseases,whereas the usage of the immunomodulators is always limited by various factors such as susceptibility to digestion by enzymes in vivo,poor penetration across biological barriers,and rapid clearance by the reticuloendothelial system.Drug delivery strategies are potent to promote their delivery.Herein,we reviewed the potential targets for immunotherapy against the major infammatory diseases,discussed the biologics and drug delivery systems involved in the immunotherapy,particularly highlighted the approved therapy tactics,and finally offer perspectives in this feld. | Qingqing Xiao Xiaotong Li Yi Li Zhenfeng Wu Chenjie Xu Zhongjian Chen Wei He | 2021 | Acta Pharmaceutica Sinica B2021，11，4： | 15 |
| 16 | Hawthorn Extract Alleviates Atherosclerosis through Regulating Inflammation and Apoptosis Related Factors: An Experimental Study显示文摘Objective: To determine the effects of hawthorn extract on serum lipid levels, pathological changes in aortic atherosclerosis plaque, inflammatory factors, and apoptosis-related protein and mRNA expression in apolipoprotein E gene knockout(ApoE^(-/-)) mice. Methods: Thirty-six ApoE^(-/-) mice were fed with a high-fat diet starting at the age of 8 weeks. Mice were randomly divided into 3 groups by a random number table including model group, hawthorn extract group, and simvastatin group, 12 mice in each group. Twelve 8-week-old C57BL/6 mice were fed a basic diet and served as control. The mice in the control and model groups were administered 0.2 mL saline daily, the mice in the hawthorn extract and simvastatin groups were administered with 50 mg/kg hawthorn extract or 5 mg/kg simvastatin daily for 16 weeks. After 16 weeks, plasma lipids including total cholesterol(TC), triglyceride(TG), low-density lipoprotein cholesterol(LDL-C) and high-density lipoprotein cholesterol(HDL-C) were determined by an enzymatic assay. Aortic atherosclerotic lesions were observed by light microscopy, scanning and transmission electron microscopy, respectively. Plasma levels of monocyte chemoattractant protein-1(MCP-1), interleukin-1β(IL-1β), adiponectin(APN), and hypersensitive C-reactive protein(hs-CRP) were measured by enzyme-linked immunosorbent assay(ELISA). Protein and mRNA expressions of Bax and Bcl-2 in the aorta were assessed by Western blotting and quantitative real-time polymerase chain reaction(qR T-PCR), respectively. Results: Compared to the control group, the plasma levels of TC, TG and LDL-C were significantly increased and HDL-C were significantly decreased in the model group(P<0.01). Compared to the model group, treatment with hawthorn extract significantly decreased the plasma levels of TC, TG, and LDL-C and increased the plasma level of HDL-C in ApoE^(-/-)mice(P<0.01). The levels of MCP-1, IL-1β, and hs-CRP in the model group were significantly increased and APN was significantly decreased compared with the control group(P<0.01). Compared to the model group, treatment with hawthorn extract decreased the levels of MCP-1, IL-1β, and hs-CRP and increased the APN level(P<0.01). Compared to the control group, the protein and mR NA expression of Bax in the model group were significantly increased and the expression of Bcl-2 was significantly decreased(P<0.01). Hawthorn extract also reduced the protein and mR NA expression of Bax and increased the Bcl-2 expression in the aorta(P<0.01). Conclusion: Hawthorn extract has anti-atherosclerosis and stabilizing unstable plaque effects. The mechanism may be related to the inflammation and apoptosis signaling pathways. | WANG Song-zi WU Min CHEN Ke-ji LIU Yue SUN Jing SUN Zhuo MA He LIU Long-tao | 2019 | Chinese Journal of Integrative Medicine2019，25，2： | 15 |
| 17 | Genetics of coronary artery disease and myocardial infarction显示文摘Atherosclerotic coronary artery disease(CAD) comprises a broad spectrum of clinical entities that include asymptomatic subclinical atherosclerosis and its clinical complications, such as angina pectoris, myocardial infarction(MI) and sudden cardiac death. CAD continues to be the leading cause of death in industrialized society. The long-recognized familial clustering of CAD suggests that genetics plays a central role in its development, with the heritability of CAD and MI estimated at approximately 50% to 60%. Understanding the genetic architecture of CAD and MI has proven to be difficult and costly due to the heterogeneity of clinical CAD and the underlying multi-decade complex pathophysiological processes that involve both genetic and environmental interactions. This review describes the clinical heterogeneity of CAD and MI to clarify the disease spectrum in genetic studies, provides a brief overview of the historical understanding and estimation of the heritability of CAD and MI, recounts major gene discoveries of potential causal mutations in familial CAD and MI, summarizes CAD and MIassociated genetic variants identified using candidate gene approaches and genome-wide association studies(GWAS), and summarizes the current status of the construction and validations of genetic risk scores for lifetime risk prediction and guidance for preventive strategies. Potential protective genetic factors against the development of CAD and MI are also discussed. Finally, GWAS have identified multiple genetic factors associated with an increased risk of in-stent restenosis following stent placement for obstructive CAD. This review will also address genetic factors associated with in-stent restenosis, which may ultimately guide clinical decision-making regarding revascularization strategies for patients with CAD and MI. | Xuming Dai Szymon Wiernek James P Evans Marschall S Runge | 2016 | World Journal of Cardiology2016，8，1： | 15 |
| 18 | Nonalcoholic fatty liver disease and aging: Epidemiology to management显示文摘Nonalcoholic fatty liver disease(NAFLD) is common in the elderly, in whom it carries a more substantial burden of hepatic(nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma) and extra-hepatic manifestations and complications(cardiovascular disease, extrahepatic neoplasms) than in younger age groups. Therefore, proper identification and management of this condition is a major task for clinical geriatricians and geriatric hepatologists. In this paper, the epidemiology and pathophysiology of this condition are reviewed, and a full discussion of the link between NAFLD and the aspects that are peculiar to elderly individuals is provided; these aspects include frailty, multimorbidity, polypharmacy and dementia. The proper treatment strategy will have to consider the peculiarities of geriatric patients, so a multidisciplinary approach is mandatory. Non-pharmacological treatment(diet and physical exercise) has to be tailored individually considering the physical limitations of most elderly people and the need for an adequate caloric supply. Similarly, the choice of drug treatment must carefully balance the benefits and risks in terms of adverse events and pharmacological interactions in the common context of both multiple health conditions and polypharmacy. In conclusion, further epidemiological and pathophysiological insight is warranted. More accurate understanding of the molecular mechanisms of geriatric NAFLD will help in identifying the most appropriate diagnostic and therapeutic approach for individual elderly patients. | Marco Bertolotti Amedeo Lonardo Chiara Mussi Enrica Baldelli Elisa Pellegrini Stefano Ballestri Dante Romagnoli Paola Loria | 2014 | World Journal of Gastroenterology2014，20，39： | 15 |
| 19 | Animal models of atherosclerosis显示文摘In this mini-review several commonly used animal models of atherosclerosis have been discussed.Among them,emphasis has been made on mice,rabbits,pigs and non-human primates.Although these animal models have played a significant role in our understanding of induction of atherosclerotic lesions,we still lack a reliable animal model for regression of the disease.Researchers have reported several genetically modified and transgenic animal models that replicate human atherosclerosis,however each of current animal models have some limitations.Among these animal models,the apolipoprotein(apo) E-knockout(KO)mice have been used extensively because they develop spontaneous atherosclerosis.Furthermore,atherosclerotic lesions developed in this model depending on experimental design may resemble humans' stable and unstable atherosclerotic lesions.This mouse model of hypercholesterolemia and atherosclerosis has been also used to investigate the impact of oxidative stress and inflammation on atherogenesis.Low density lipoprotein(LDL)-r-KO mice are a model of human familial hypercholesterolemia.However,unlike apo E-KO mice,the LDL-r-KO mice do not develop spontaneous atherosclerosis.Both apo E-KO and LDL-r-KO mice have been employed to generate other relevant mouse models of cardiovascular disease through breeding strategies.In addition to mice,rabbits have been used extensively particularly to understand the mechanisms of cholesterol-induced atherosclerosis.The present review paper details the characteristics of animal models that are used in atherosclerosis research. | Fatemeh Ramezani Kapourchali Gangadaran Surendiran Li Chen Elisabeth Uitz Babak Bahadori Mohammed H Moghadasian | 2014 | World Journal of Clinical Cases2014，2，5： | 14 |
| 20 | Pathogenesis and significance of hepatitis C virus steatosis:An update on survival strategy of a successful pathogen显示文摘Hepatitis C virus(HCV)is a successful pathogen on the grounds that it exploits its host’s metabolism to build up viral particles;moreover it favours its own survival by inducing chronic disease and the development of specific anatomic changes in the infected organ.Steatosis,therefore,is associated with HCV infection by necessity rather than by chance alone.Approximately6%of HCV patients have steatohepatitis.Interestingly,HCV steatosis occurs in the setting of multiple metabolic abnormalities(hyperuricemia,reversible hypocholesterolemia,insulin resistance,arterial hypertension and expansion of visceral adipose tissue)collectively referred to as'hepatitis C-associated dysmetabolic syndrome'(HCADS).General,nonalcoholic fatty liver disease(NAFLD)-like,mechanisms of steatogenesis(including increased availability of lipogenic substrates and de novo lipogenesis;decreased oxidation of fatty substrates and export of fatty substrates)are shared by all HCV genotypes.However,genotype 3 seemingly amplifies such steatogenic molecular mechanisms reported to occur in NAFLD via more profound changes in microsomal triglyceride transfer protein;peroxisome proliferator-activated receptor alpha;sterol regulatory element-binding proteins and phosphatase and tensin homologue.HCV steatosis has a remarkable clinical impact in as much as it is an acknowledged risk factor for accelerated fibrogenesis;for impaired treatment response to interferon and ribavirin;and development of hepatocellular carcinoma.Recent data,moreover,suggest that HCV-steatosis contributes to premature atherogenesis via both direct and indirect mechanisms.In conclusion,HCV steatosis fulfills all expected requirements necessary to perpetuate the HCV life cycle.A better understanding of the physiology of HCADS will likely result in a more successful handling of disease with improved antiviral success rates. | Amedeo Lonardo Luigi Elio Adinolfi Luciano Restivo Stefano Ballestri Dante Romagnoli Enrica Baldelli Fabio Nascimbeni Paola Loriaca | 2014 | World Journal of Gastroenterology2014，20，23： | 14 |
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