Future lipidology最新文献

{"title":"Oxidized LDL and the metabolic syndrome.","authors":"Paul Holvoet, Dieuwke De Keyzer, David R Jacobs","doi":"10.2217/17460875.3.6.637","DOIUrl":"10.2217/17460875.3.6.637","url":null,"abstract":"<p><p>The metabolic syndrome is a common and complex disorder combining obesity, dyslipidemia, hypertension and insulin resistance. It is associated with a high cardiovascular risk that can only partially be explained by its components. There is evidence that low-grade inflammation and high oxidative stress add to this risk. Oxidized LDL, a marker of lipoprotein-associated oxidative stress, is an emerging cardiovascular risk factor. In this review, we demonstrate that the metabolic syndrome exacerbates oxidized LDL in a feedback loop. We introduce molecular mechanisms underlying this loop. Finally, we demonstrate that weight loss and statin treatment lower metabolic syndrome factors associated with a reduction of oxidized LDL. The current data warrant further investigation into the role of lifestyle and therapeutic interventions that inhibit tissue-associated oxidation of LDL in the prevention of the metabolic syndrome.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":" ","pages":"637-649"},"PeriodicalIF":0.0,"publicationDate":"2008-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631666/pdf/nihms88118.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40054848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of phosphoethanolamine-bound C-reactive protein in atherosclerosis.","authors":"Alok Agrawal","doi":"10.2217/17460875.3.6.599","DOIUrl":"https://doi.org/10.2217/17460875.3.6.599","url":null,"abstract":"Three papers published in the year 2008 from my laboratory reported experiments and data indicating the therapeutic potential of phosphoethanolamine-bound C-reactive protein (PEt-bound CRP) in atherosclerosis. The small-molecule compound PEt, which binds to CRP, could in itself be of therapeutic value. The first paper described the capability of PEt-bound CRP to capture native low-density lipoprotein (LDL) cholesterol in human serum [1]. The second paper described the potency of PEt-bound CRP to bind to a modified form of LDL called enzymatically-modified LDL (E-LDL). Although CRP alone could bind to E-LDL, the PEt-bound CRP was much more potent than unbound CRP in binding to E-LDL [2]. This paper also reported a previously unknown function of CRP. CRP, once bound to E-LDL, prevented the formation of E-LDL-loaded macrophage foam cells. The third paper further emphasized the importance of PEt-bound CRP and presented a review of the literature on the connection between CRP and atherosclerosis [3]. CRP, also known as high-sensitivity CRP or hsCRP, is a serum protein which is used as a marker of systemic inflammation [see CRP reviews 3-7, and the references cited in 3, 4]. CRP is associated with risk of atherosclerosis; however, recent data suggest that the association of CRP with atherosclerosis may not be causal [8]. In 1982, it was shown that under certain experimental conditions CRP interacted with LDL [9]. Since then CRP was suspected to play a role in atherosclerosis. CRP was also found deposited and co-localized with LDL and macrophages in human atherosclerotic lesions. Discovering the functions of CRP in atherosclerosis quickly became a hot subject for research. Atherosclerosis is a heart disease caused by the deposition and subsequent modification of LDL in artery walls. Atherogenic LDL, which includes modified forms of LDL produced by oxidation and proteolysis of LDL, enters macrophages to form foam cells. The LDL-loaded macrophage foam cells contribute to the development of atherosclerosis which leads to myocardial infarction. To prevent atherosclerosis, LDL can be targeted therapeutically at two locations: the native LDL found mostly in the circulation and the atherogenic LDL located mostly in the artery walls.","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":"3 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2008-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/17460875.3.6.599","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31976539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sphingosine-1-phosphate synthesis and functions in mast cells.","authors":"Megan M Price, Carole A Oskeritzian, Sheldon Milstien, Sarah Spiegel","doi":"10.2217/17460875.3.6.665","DOIUrl":"10.2217/17460875.3.6.665","url":null,"abstract":"<p><p>Sphingolipids are not only major lipid components of all eukaryotic cell membranes, but they also comprise an important family of bioactive signaling molecules that regulate a diverse array of biological responses. The sphingolipid metabolite sphingosine-1-phosphate (S1P), is a key regulator of immune responses. Cellular levels of S1P are determined by the balance between its synthesis, involving two sphingosine kinases (SphK1 and SphK2), and its degradation, involving S1P lyase and S1P phosphatases. S1P mainly signals through its cell-surface receptors and may also have intracellular functions. S1P has important functions in mast cells - the major effectors of allergic responses. Antigen triggering of IgE receptors on mast cells activates both SphKs resulting in the production of S1P that is released and regulates and amplifies mast cell functions, including degranulation as well as cytokine and chemokine release.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":" ","pages":"665-674"},"PeriodicalIF":0.0,"publicationDate":"2008-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2749270/pdf/nihms88122.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40054423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Augmentation of the renin-angiotensin system by hypercholesterolemia promotes vascular diseases.","authors":"Alan Daugherty, Hong Lu, Debra L Rateri, Lisa A Cassis","doi":"10.2217/17460875.3.6.625","DOIUrl":"10.2217/17460875.3.6.625","url":null,"abstract":"<p><p>Activation of the renin-angiotensin system (RAS) and aberrant cholesterol metabolism have generally been considered as independent mechanisms in the development of several vascular diseases. However, it is becoming increasingly apparent in both human and animal studies that many aspects of the RAS may be augmented by hypercholesterolemia, resulting in enhancement of the severity and occurrence of several vascular diseases, including hypertension, atherosclerosis and abdominal aortic aneurysms. Some potential hypercholesterolemia-induced mechanisms have been demonstrated to increase activity of specific components of the RAS. These include increased AT1-receptor expression, increased responsiveness to Ang II and increased synthesis of angiotensin peptides. Future studies need to validate mechanisms of hypercholesterolemia-induced RAS activation in different vascular diseases.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":" ","pages":"625-636"},"PeriodicalIF":0.0,"publicationDate":"2008-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2636897/pdf/nihms88119.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40054767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apolipoprotein E and cholesterol in aging and disease in the brain.","authors":"Elena Posse de Chaves, Vasanthy Narayanaswami","doi":"10.2217/17460875.3.5.505","DOIUrl":"10.2217/17460875.3.5.505","url":null,"abstract":"<p><p>Cholesterol can be detrimental or vital, and must be present in the right place at the right time and in the right amount. This is well known in the heart and the vascular system. However, in the CNS cholesterol is still an enigma, although several of its fundamental functions in the brain have been identified. Brain cholesterol has attracted additional attention owing to its close connection to ApoE, a key polymorphic transporter of extracellular cholesterol in humans. Indeed, both cholesterol and ApoE are so critical to fundamental activities of the brain, that the brain regulates their synthesis autonomously. Yet, similar control mechanisms of ApoE and cholesterol homeostasis may exist on either sides of the blood-brain barrier. One indication is that the APOE ε4 allele is associated with hypercholesterolemia and a proatherogenic profile on the vascular side and with increased risk of Alzheimer's disease on the CNS side. In this review, we draw attention to the association between cholesterol and ApoE in the aging and diseased brain, and to the behavior of the ApoE4 protein at the molecular level. The attempt to correlate in vivo and in vitro observations is challenging but crucial for developing future strategies to address ApoE-related aberrations in cholesterol metabolism selectively in the brain.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":" ","pages":"505-530"},"PeriodicalIF":0.0,"publicationDate":"2008-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600507/pdf/nihms72621.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40006025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of Eicosanoids in Prostate Cancer.","authors":"Kasem Nithipatikom,&nbsp;William B Campbell","doi":"10.2217/17460875.3.4.453","DOIUrl":"https://doi.org/10.2217/17460875.3.4.453","url":null,"abstract":"<p><p>Eicosanoids, the metabolites of arachidonic acid, have diverse functions in the regulation of cancer including prostate cancer. This review will provide an overview of the roles of eicosanoids and endocannabinoids and their potential as therapeutic targets for prostate cancer treatment.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":"3 4","pages":"453-467"},"PeriodicalIF":0.0,"publicationDate":"2008-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/17460875.3.4.453","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32148432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ceramide signaling in cancer and stem cells.","authors":"Erhard Bieberich","doi":"10.2217/17460875.3.3.273","DOIUrl":"10.2217/17460875.3.3.273","url":null,"abstract":"<p><p>Most of the previous work on the sphingolipid ceramide has been devoted to its function as an apoptosis inducer. Recent studies, however, have shown that in stem cells, ceramide has additional nonapoptotic functions. In this article, ceramide signaling will be reviewed in light of 'systems interface biology': as an interconnection of sphingolipid metabolism, membrane biophysics and cell signaling. The focus will be on the metabolic interconversion of ceramide and sphingomyelin or sphingosine-1-phosphate. Lipid rafts and sphingolipid-induced protein scaffolds will be discussed as a membrane interface for lipid-controlled cell signaling. Ceramide/sphingomyelin and ceramide/sphingosine-1-phosphate-interdependent cell-signaling pathways are significant for the regulation of cell polarity, apoptosis and/or proliferation, and as novel pharmacologic targets in cancer and stem cells.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":"3 3","pages":"273-300"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493052/pdf/nihms54187.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27873707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage infiltration into adipose tissue: initiation, propagation and remodeling.","authors":"Bonnie K Surmi, Alyssa H Hasty","doi":"10.2217/17460875.3.5.545","DOIUrl":"https://doi.org/10.2217/17460875.3.5.545","url":null,"abstract":"<p><p>It has long been known that adipose tissue in obesity is in a heightened state of inflammation. Recently, our understanding of this has been transformed by the knowledge that immune cells such as macrophages and T cells can infiltrate adipose tissue and are responsible for the majority of inflammatory cytokine production. These seminal findings have opened up a new area in biology that is garnering the interest of scientists involved in research relating to cell motility, inflammation, obesity, physiology, diabetes and cardiovascular disease. Some important general questions relevant to this field are: how are macrophages recruited to adipose tissue in obesity? What are the physiological consequences of macrophage-adipocyte interactions? Do these inflammatory macrophages contribute to pathophysiological conditions associated with obesity, such as insulin resistance, dyslipidemia, diabetes and cardiovascular disease? This review focuses on the first of these important questions.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":"3 5","pages":"545-556"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uncontrolled airway inflammation in lung disease represents a defect in counter-regulatory signaling.","authors":"Anna Planaguma, Bruce D Levy","doi":"10.2217/17460875.3.6.697","DOIUrl":"10.2217/17460875.3.6.697","url":null,"abstract":"<p><p>Counter-regulatory lipid mediators are generated during airway inflammation to promote resolution. Defects in the production of these lipid mediators have now been associated with several diseases of persistent airway inflammation. Lipoxins are the lead members of this class of anti-inflammatory and proresolving chemical mediators. Recently, several new families of fatty acid-derived counter-regulatory mediators have been discovered, including the resolvins and protectins. Diminished formation of these endogenous protective signals would interrupt the natural resolution of inflammation. Here, we review how rapidly emerging information on lipoxins, resolvins and protectins is providing new insights into the pathophysiology of chronic airway inflammation in several common illnesses, including asthma.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":"3 6","pages":"697-704"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2655728/pdf/nihms-88121.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28050292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-chain acyl-CoA synthetases and fatty acid channeling.","authors":"Douglas G Mashek, Lei O Li, Rosalind A Coleman","doi":"10.2217/17460875.2.4.465","DOIUrl":"10.2217/17460875.2.4.465","url":null,"abstract":"<p><p>Thirteen homologous proteins comprise the long-chain acyl-CoA synthetase (ACSL), fatty acid transport protein (FATP), and bubblegum (ACSBG) subfamilies that activate long-chain and very-long-chain fatty acids to form acyl-CoAs. Gain- and loss-of-function studies show marked differences in the ability of these enzymes to channel fatty acids into different pathways of complex lipid synthesis. Further, the ability of the ACSLs and FATPs to enhance cellular FA uptake does not always require these proteins to be present on the plasma membrane; instead, FA uptake can be increased by enhancing its conversion to acyl-CoA and its metabolism in downstream pathways. Since altered fatty acid metabolism is a hallmark of numerous metabolic diseases and pathological conditions, the ACSL, FATP and ACSBG isoforms are likely to play important roles in disease etiology.</p>","PeriodicalId":87611,"journal":{"name":"Future lipidology","volume":"2 4","pages":"465-476"},"PeriodicalIF":0.0,"publicationDate":"2007-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846691/pdf/nihms179818.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28889831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}