|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Regulation and deregulation of cholesterol homeostasis: The liver as a metabolic 'power station'显示文摘Cholesterol plays several structural and metabolic roles that are vital for human biology. It spreads along the entire plasma membrane of the cell, modulating fluidity and concentrating in specialized sphingolipid-rich domains called rafts and caveolae. Cholesterol is also a substrate for steroid hormones. However, too much cholesterol can lead to pathological pictures such as atherosclerosis, which is a consequence of the accumu- lation of cholesterol into the cells of the artery wall. The liver is considered to be the metabolic power station of mammalians, where cholesterol homeostasis relies on an intricate network of cellular processes whose deregulations can lead to several life-threatening pathologies, such as familial and age-related hypercholesterolemia. Cholesterol homeostasis maintenance is carried out by: biosynthesis, via 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity; uptake, through low density lipoprotein receptors (LDLr); lipoprotein release in the blood; storage by esterification; and degradation and conversion into bile acids. Both HMGR and LDLr are transcribed as a function of cellular sterol amount by a family of transcription factors called sterol regulatory element binding proteins that are responsible for the maintenance of cholesterol homeostasis through an intricate mechanism of regulation. Cholesterol obtained by hepatic de novo synthesis can be esterified and incorporated into apolipoprotein B-100-containing very low density lipoproteins, which are then secreted into the bloodstream for transport to peripheral tissues. Moreover, dietary cholesterol is transferred from the intestine to the liver by high density lipoproteins (HDLs); all HDL particles are internalized in the liver, interacting with the hepatic scavenger receptor (SR-B1). Here we provide an updated overview of liver cholesterol metabolism regulation and deregulation and the causes of cholesterol metabolism-related diseases. Moreover, current pharmacological treatment and novel hypocho-lesterolemic strategies will also be introduced. | Laura Trapani Marco Segatto Valentina Pallottini | 2012 | World Journal of Hepatology2012，4，6： | 5 |
| 2 | New compounds able to control hepatic cholesterol metabolism:Is it possible to avoid statin treatment in aged people?显示文摘Aging is characterized by the loss of homeostasis that leads to changes in the biochemical composition of tissues, reduced ability to respond adaptively to en- vironmental stimuli, and increased susceptibility and vulnerability to diseases including coronary artery dis- eases, carotid artery disease and brain vessel disease. Hypercholesterolemia is one of the primary risk factors for these pathologies, whose incidence is highly related to aging. Almost 25% of men and 42% of women older than 65 years have a serum total cholesterol level greater than 240 mg/dL. The mechanisms behind this age-related increase in plasma cholesterol are still incompletely understood, thus, the control of plasma cholesterol content in aged people is more challenging than in adults. In this review the different pharmaco- logical approaches to reduce plasma cholesterol levels, particularly in aged people, will be discussed. In brief, current therapies are mostly based on the prescription of statins(3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) that are pretty effective but that exert sev- eral side effects. More attention should be given to po- tential drug interactions, potential age-related changes in drug pharmacokinetics, adverse effects such as my-opathy and competing risks when statins are prescribed to old patients. In combination or in alternative to sta- tin therapy, other agents might be required to reduce low density lipoprotein(LDL) cholesterol levels. Among the available drugs, the most commonly prescribed are those addressed to reduce cholesterol absorption, to modulate lipoprotein lipase activity and bile acid se- questrants: even these pharmacological interventions are not exempt from side effects. The use of antioxi- dants or organoselenium compounds and the discovery of new proteins able to modulate exclusively LDL re- ceptor recycling such as Proprotein convertase subtilisin kexin 9 and SEC24 offer new pharmacological approaches to selectively reduce the main causes of dyslipidemia. | Laura Trapani Marco Segatto Valentina Pallottini | 2013 | World Journal of Hepatology2013，5，12： | 2 |
| 3 | Constitutively active Notchl induces growth arrest of HPV-positive cervical cancer cells via separate signaling pathways显示文摘 | Talora C Cialfi S Segatto O | 2005 | Exp Cell Res2005，305，2： | 1 |
| 4 | Constitutively active Notch1 induces growth arrest of HPV-positive cervical cancer cells via separate signaling pathways显示文摘 | Talora C Cialfi S Segatto O | 2005 | Exp Cell Res2005，305，2： | 1 |
| 5 | A band-width scalable OFDM passive optical network for future access network显示文摘 | Coura 1B J C Silva JA L Segatto M E V | 2009 | Photonic Network Communications2009，18，3： | 1 |
| 6 | Constitutively active Notchl induces growth arrest of HPV-positive cervical cancer cells via separate signaling pathways 显示文摘 | Talora C Cialfi S Segatto O | 2005 | Exp Cell Res2005，305，2： | 1 |
| 7 | Constitutively active Notch1 induces growth arrest of HPV-positive cervical cancer cells via separate signaling pathways显示文摘 | Talora C Cialfi S Segatto O | 2005 | Exp Cell Res2005，305，2： | 1 |
| 8 | Constitutively active Notchl induces growth arrest of HPV-positive cervical cancer ceils via separate sig- naling pathways 显示文摘 | Talora C Cialfi S Segatto O | 2005 | Exp Cell Res2005，305，2： | 1 |
| 9 | The infected liver:radiologic-pathologic correlation显示文摘 | Mortele KJ Segatto E Ros PR | 2004 | Radiographics2004，24，： | 1 |
| 10 | Computed tomography featuresof nonalcoholic steatohepatitis with histopathologic correlation显示文摘 | Oliva MR Mortele KJ Segatto E | 2006 | JComput Assist Tomogr2006，30，1： | 1 |
| 11 | Lipodystro- phy in HIV/AIDS patients with different levels of physical activity while on antiretroviral therapy 显示文摘 | Segatto AF Freitas Junior IF Samos VR | 2011 | Rev Soc Bras Med Trop2011，44，4： | 1 |
| 12 | Interruption of measles transmission in Brazil, 2000-2001 显示文摘 | Prevots DR Parise MS Segatto TC | 2003 | Journal of infectious Diseases2003，187，1： | 1 |
| 13 | Computed tomography features of nonalcoholic steatohepatitis with histopathologic correlation显示文摘 | Oliva M R Mortele K J Segatto E | 2006 | J Comput Assist Tomogr2006，30，1： | 1 |
| 14 | Constitutively active Notchlinduces growth arrest of HPV -positive cervical cancer cells viaseparate signaling pathways 显示文摘 | Talora C Cialfi S Segatto 0 | 2005 | Exp Cell Res2005，305，： | 1 |
| 15 | Constitutively active Notch1 induces growth arrest of HPV-positive cervical cancer cells via separate signaling pathways显示文摘 | Talora C Cialfi S Segatto O | 2005 | Exp Cell Res2005，305，2： | 1 |
| 16 | Craniofacial features of children with spinal deformities显示文摘 | Segatto E Lippold C Vegh A | 2008 | BMC Musculoskelet Disord2008，9，： | 1 |
| 17 | Computed to mography fea- tures of nonalcoholic teatohepatitis with histopa thologiccorre-lation 显示文摘 | liverdisea- Oliva MR Mortele KJ Segatto E | 2006 | J Comput Assist Tomogr2006，30，1： | 1 |
| 18 | Acute small bowel ischemia:CT imaging finding显示文摘 | Segatto E Mortele KJ Ji H | 2003 | Semin Ultrasound CT MRI2003，24，5： | 1 |
| 19 | Abandwidth scalable OFDM passive optical network forfuture access network显示文摘 | COURA D J C SILVA J A L SEGATTO M E V | 2009 | Photon Netw Commun2009，18，3： | 1 |
| 20 | The Infected Liver:Radiologic -Pathologic Correlation显示文摘 | Koenraad J Mortele Enrica Segatto Pablo R Ros | 2004 | RadioGraphics2004，24，4： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员