检索结果-南通市图书馆

fibrogenesis and fibrosis in inflammatory bowel diseases:Good and bad side of same coin?

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastrointestinal Pathophysiology 2013年第4期4卷 100-107页

作者： Mariabeatrice Principi Floriana Giorgio Giuseppe Losurdo Viviana Neve Antonella Contaldo Alfredo Di Leo Enzo Ierardi Gastroenterology Department of Emergency and Organ TransplantationUniversity of Bari

fibrogenesis in inflammatory bowel diseases is a complex phenomenon aimed at mucosal repair. However, it may provoke intestinal fibrosis with the development of strictures which require surgery. Therefore, fibrogenesis may be considered as a 'two-faced' process when related to chronic intestinal inflammation. Many types of cells may be converted into the fibrogenic phenotype at different levels of the intestinal wall. A complex interaction of cytokines, adhesion molecules and growth factors is involved in the process. We report an overview of recent advances in molecular mechanisms of stricturizing Crohn’s disease(CD) including the potential role of trasforming growth factor beta, protein kinase C and Ras, Raf and ERK proteins. Fibrotic growth factors such as vascular endothelial growth factor and platelet-derived growth factor, as well as the Endothelial-to-Mesenchymal Transition induced by transforming growth factor-β, are considered. Finally, our experience, focused on tumor necrosis factor α(the main cytokine of inflammatory bowel diseases) and the link between syndecan 1(a heparan sulphate adhesion molecule) and basic fibroblast growth factor(a strong stimulator of collagen synthesis) is described. We hypothesize a possible molecular pattern for mucosal healing as well as how its deregulation could be involved in fibrotic complications of CD. A final clinical point is the importance of performing an accurate evaluation of the presence of fibrotic strictures before starting anti-tumor necrosis α treatment, which could worsen the lesions.

关键词： fibrogenesis Fibrosis Tumor necrosis factor-α Syndecan 1 Basic fibroblast growth factor Cellular fibrogenic phenotype Inflammatory bowel diseases

fibrogenesis in inflammatory bowel disease——A bright road ahead

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

中华炎性肠病杂志（中英文） 2018年第1期2卷 3-4页

作者： Florian Rieder Claudio Fiocchi Department of Pathobiology Lerner Research InstituteDepartment of GastroenterologyHepatology and Nutrition Digestive Disease and Surgery Institute Cleveland ClinicClevelandUSA

Intestinal fibrosis is a frequent complication of inflammatory bowel diseases (IBD),and can lead to stricture formation and intestinal obstruction. Clinically apparent stenosis occurs in more than 30% of patients with Crohn's disease (CD) and about 5%~10% of patients with ulcerative colitis (UC) [l -2],and its management represents an important and frequent challenge in clinical practice. Despite its tremendous clinical impact the tools we currently have to address this challenge are limited (l)Anti-inflammatory therapies are only a temporizing measure to relieve obstruction and re-obstruction is frequent, necessitating endoscopic balloon dilation or surgical intervention(3 5)No specific anti-fibrotic therapy exists at present, and therefore it is critical to understand the mechanisms of intestinal fibrogenesis to develop targeted therapeutic approaches.

关键词： fibrogenesis ahead stenosis

Hepatocellular carcinoma in nonalcoholic fatty liver: Role of environmental and genetic factors

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2014年第36期20卷 12945-12955页

作者： Paola Dongiovanni Stefano Romeo Luca Valenti Internal Medicine 1B Fondazione IRCCS Ca’ Granda Ospedale Policlinico 20122 Milano Italy Department of Pathophysiology and Transplantation Università degli Studi di Milano 20122 Milano Italy Wallenberg Laboratory Department of Molecular and Clinical Medicine University of Gothenburg 40530 Gothenburg Sweden Clinical Nutrition Unit Department of Medical and Surgical Sciences University Magna Graecia 88100 Catan-zaro Italy

Hepatocellular carcinoma(HCC) is the fourth cause of cancer related mortality, and its incidence is rapidly increasing. Viral hepatitis, alcohol abuse, and exposure to hepatotoxins are major risk factors, but nonalcoholic fatty liver disease(NAFLD) associated with obesity, insulin resistance, and type 2 diabetes, is an increasingly recognized trigger, especially in developed countries. Older age, severity of insulin resistance and diabetes, and iron overload have been reported to predispose to HCC in this context. Remarkably, HCCs have been reported in non-cirrhotic livers in a higher proportion of cases in NAFLD patients than in other etiologies. Inherited factors have also been implicated to explain the different individual susceptibility to develop HCC, and their role seems magnified in fatty liver, where only a minority of affected subjects progresses to cancer. In particular, the common I148 M variant of the PNPLA3 gene influencing hepatic lipid metabolism influences HCC risk independently of its effect on the progression of liver fibrosis. Recently, rare loss-of-function mutations in Apolipoprotein B resulting in very low density lipoproteins hepatic retention and in Telomerase reverse transcriptase influencing cellular senescence have also been linked to HCC in NAFLD. Indeed, hepatic stellate cells senescence has been suggested to bridge tissue aging with alterations of the intestinal microbiota in the pathogenesis of obesity-related HCC. A deeper understanding of the mechanisms mediating hepatic carcinogenesis during insulin resistance, and the identification of its genetic determinants will hopefully provide new diagnostic and therapeutic tools.

关键词： Nonalcoholic fatty liver disease Steatosis Hepatocellular carcinoma Cirrhosis fibrogenesis Liver disease Genetics Single nucleotide polymorphism Patatin-like phospholipase domain-containing 3

Osteopontin is an important mediator of alcoholic liver disease via hepatic stellate cell activation

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2014年第36期20卷 13088-13104页

作者： Devanshi Seth Alastair Duly Paul C Kuo Geoffrey W McCaughan Paul S Haber Drug Health Services Royal Prince Alfred Hospital Camperdown NSW 2050 Australia Garvan Institute Darlinghurst NSW 2010 Australia Central Clinical School of Medicine the University of Sydney Sydney NSW 2050 Australia Department of Surgery Loyola University Medica Centre Maywood IL 60153 United States AW Morrow Gastroenterology and Liver Centre RPAH Camperdown NSW 2050 Australia

AIM: To investigate over-expression of Osteopontin (OPN) pathway expression and mechanisms of action in human alcoholic liver disease (ALD), in vivo and in vitro acute alcohol models.

关键词： Hepatic stellate cells Liver cirrhosis Plasmin Steatosis fibrogenesis Transforming growth factor β Osteopontin isoform

Iron metabolism disorders in patients with hepatitis B-related liver diseases

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Clinical Cases 2018年第13期6卷 600-610页

作者： Yan-Hang Gao Jing-Yun Wang Pei-Yan Liu Jing Sun Xiao-Mei Wang Rui-Hong Wu Xiu-Ting He Zheng-Kun Tu Chun-Guang Wang Hong-Qin Xu Jun-Qi Niu Department of Hepatology The First Hospital of Jilin University Jilin University Department of Gastroenterology Weihaiwei People’s Hospital Department of Gastroenterology Heping Hospital Changzhi Medical College Department of Geriatrics The First Hospital of Jilin University Department of Translational Medicine The First Hospital of Jilin University Department of Surgery The Second Hospital of Jilin University Jilin Provincial Key Laboratory of Infectious Diseases Laboratory of Molecular Virology

AIM To investigate the relationship between levels of iron metabolism markers and hepatitis B virus(HBV)-related chronic liver *** This case-control study with 318 participants included 78 cases of chronic hepatitis B, 85 cases of HBV-related liver cirrhosis, 77 cases of HBV-related hepatocellular carcinoma, and 78 healthy controls. Markers of iron metabolism were detected in participants. Hematological and biochemical parameters and HBV-DNA were assessed. Child-Pugh grade and Barcelona Clinic Liver Cancer stage were determined for each hepatocellular carcinoma patient. Perls' staining was performed on liver sections. The SPSS program was used for all statistical analyses, and statistical significance was considered if a P-value < *** Significantly higher serum ferritin and lower serum hepcidin levels were detected in all groups of HBV-infected patients compared with healthy controls. Serum iron, total iron binding capacity, and serum transferrin levels were significantly lower in patients with cirrhosis and hepatocellular carcinoma, whereas the hepcidin level was higher than that in chronic hepatitis B patients. Correlation analysis indicated that serum hepcidin was negatively correlated with HBV-DNA load(P < 0.01). Serum ferritin and transferrin saturation levels increased proportionally to the extent of liver cirrhosis and poorer Child-Pugh scores(P < 0.05). The decreased serum iron and transferrin saturation levels were significantly correlated with a smaller hepatocellular carcinoma tumor burden according to Barcelona Clinic Liver Cancer staging. Liver histology showed a clearly increasing trend in iron deposition in the liver tissues with increased fibrosis, which became prominent at stages 3(severe liver fibrosis) and 4(cirrhosis). CONCLUSION Iron metabolism disorders occur in patients with HBVrelated liver diseases. The serum markers of iron metabolism disorders vary in different stages of HBV-related liver diseases.

关键词： Hepatocellular carcinoma Hepcidin Iron staining Hepatitis B Liver fibrogenesis

Extrahepatic complications to cirrhosis and portal hypertension: Haemodynamic and homeostatic aspects

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2014年第42期20卷 15499-15517页

作者： S?ren M?ller Jens H Henriksen Flemming Bendtsen Department of Clinical Physiology and Nuclear Medicine Center for Functional and Diagnostic Imaging and Research Copenhagen University Hospital University of Copenhagen Gastro Unit Medical Division Hvidovre Hospital Hvidovre Hospital Faculty of Health Sciences University of Copenhagen

In addition to complications relating to the liver, patients with cirrhosis and portal hypertension develop extrahepatic functional disturbances of multiple organ systems. This can be considered a multiple organ failure that involves the heart, lungs, kidneys, the immune systems, and other organ systems. Progressive fibrosis of the liver and subsequent metabolic impairment leads to a systemic and splanchnic arteriolar vasodilatation. This affects both the haemodynamic and functional homeostasis of many organs and largely determines the course of the disease. With the progression of the disease, the circulation becomes hyperdynamic with cardiac, pulmonary as well as renal consequences for dysfunction and reduced survival. Infections and a changed cardiac function known as cirrhotic cardiomyopathy may be involved in further aggravation of other complications such as renal failure precipitatingthe hepatorenal *** with end-stage liver disease and related complications as for example the hepatopulmonary syndrome can only radically be treated by liver *** a bridge to this treatment,knowledge on the mechanisms of the pathophysiology of complications is essential for the choice of vasoactive drugs,antibiotics,drugs with specific effects on fibrogenesis and inflammation,and drugs that target specific receptors.

关键词： fibrogenesis Splanchnic haemodynamics Inflammation Bacterial translocation Infections Systemic circulation Cirrhotic cardiomyopathy Hepatopulmonary syndrome Portopulmonary hypertension Hepatorenal syndrome Ascites

Cellular and molecular mechanisms in the pathogenesis of liver fibrosis:An update

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2014年第23期20卷 7260-7276页

作者： Gülsüm ?zlem Elpek Department of Pathology Akdeniz University Medical School07070 AntalyaTurkey

There have been considerable recent advances towards a better understanding of the complex cellular and molecular network underlying liver *** data indicate that the termination of fibrogenic processes and the restoration of deficient fibrolytic pathways may allow the reversal of advanced fibrosis and even ***,efforts have been made to better clarify the cellular and molecular mechanisms that are involved in liver *** of hepatic stellate cells(HSCs)remains a central event in fibrosis,complemented by other sources of matrix-producing cells,including portal fibroblasts,fibrocytes and bone marrow-derived *** cells converge in a complex interaction with neighboring cells to provoke scarring in response to persistent *** the interaction of different cell types,revealing the effects of cytokines on these cells and characterizing the regulatory mechanisms that control gene expression in activated HSCs will enable the discovery of new therapeutic ***,the characterization of different pathways associated with different etiologies aid in the development of disease-specific *** article outlines recent advances regarding the cellular and molecular mechanisms involved in liver fibrosis that may be translated into future *** pathogenesis of liver fibrosis associated with alcoholic liver disease,non-alcoholic fatty liver disease and viral hepatitis are also discussed to emphasize the various mechanisms involved in liver fibrosis.

关键词： Liver Liver fibrosis Cirrhosis fibrogenesis Hepatic stellate cells Myofibroblast Extracellular matrix

Thrombin activation and liver inflammation in advanced hepatitis C virus infection

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2016年第18期22卷 4427-4437页

作者： Emilio González-Reimers Geraldine Quintero-Platt Candelaria Martín-González Onán Pérez-Hernández Lucía Romero-Acevedo Francisco Santolaria-Fernández Servicio de Medicina Interna Hospital Universitario de Canarias Universidad de La Laguna

Hepatitis C virus(HCV) infection is associated with increased thrombotic risk. Several mechanisms are involved including direct endothelial damage by the HCV virus, with activation of tissue factor, altered fibrinolysis and increased platelet aggregation and activation. In advanced stages, chronic HCV infection may evolve to liver cirrhosis, a condition in which alterations in the portal microcirculation may also ultimately lead to thrombin activation, platelet aggregation, and clot formation. Therefore in advanced HCV liver disease there is an increased prevalence of thrombotic phenomena in portal vein radicles. Increased thrombin formation may activate hepatic stellate cells and promote liver fibrosis. In addition, ischemic changes derived from vascular occlusion by microthrombi favor the so called parenchymal extinction, a process that promotes collapse of hepatocytes and the formation of gross fibrous tracts. These reasons may explain why advanced HCV infection may evolve more rapidly to end-stage liver disease than other forms of cirrhosis.

关键词： Coagulation Liver cirrhosis Hepatitis C virus fibrogenesis Parenchymal extinction Portal thrombosis Protein C

Integrated network analysis of transcriptomic and protein-protein interaction data in taurine-treated hepatic stellate cells

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2019年第9期25卷 1067-1079页

作者： Xing-Qiu Liang Jian Liang Xiao-Fang Zhao Xin-Yuan Wang Xin Deng Department of Science and Technology Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine College of Medical Guangxi University School of Basic Sciences Guangxi University of Chinese Medicine

BACKGROUND Studies show that the antifibrotic mechanism of taurine may involve its inhibition of the activation and proliferation of hepatic stellate cells(HSCs). Since the molecular mechanism of taurine-mediated antifibrotic activity has not been fully unveiled and is little studied, it is imperative to use "omics" methods to systematically investigate the molecular mechanism by which taurine inhibits liver *** To establish a network including transcriptomic and protein-protein interaction data to elucidate the molecular mechanism of taurine-induced HSC *** We used microarrays, bioinformatics, protein-protein interaction(PPI) network,and sub-modules to investigate taurine-induced changes in gene expression in human HSCs(LX-2). Subsequently, all of the differentially expressed genes(DEGs) were subjected to gene ontology function and Kyoto encyclopedia of genes and genomes pathway enrichment analysis. Furthermore, the interactions of DEGs were explored in a human PPI network, and sub-modules of the DEGs interaction network were analyzed using Cytoscape *** A total of 635 DEGs were identified in taurine-treated HSCs when compared with the controls. Of these, 304 genes were statistically significantly up-regulated, and 331 down-regulated. Most of these DEGs were mainly located on the membrane and extracellular region, and are involved in the biological processes of signal transduction, cell proliferation, positive regulation of extracellular regulated protein kinases 1(ERK1) and ERK2 cascade, extrinsic apoptotic signaling pathway and so on. Fifteen significantly enriched pathways with DEGs were identified, including mitogen-activated protein kinase(MAPK) signaling pathway, peroxisome proliferators-activated receptor signaling pathway,estrogen signaling pathway, Th1 and Th2 cell differentiation, cyclic adenosine monophosphate signaling pathway and so on. By integrating the transcriptomics and human PPI data, nine critical genes, inclu

关键词： Taurine Hepatic stellate cells Differentially expressed genes Liver fibrogenesis Transcriptomic Protein-protein interaction network