Relevant bibliographies by topics / Liver fibrosis progression

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Liver fibrosis progression'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Liver fibrosis progression"

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Samokhodskaia, Larisa Mikhaylovna, Ekaterina Evgen'evna Starostina, Elena Borisovna Yarovaya, Tat'yana Nikolaevna Krasnova, Nikolay Alekseevich Mukhin, Vsevolod Arsen'evich Tkachuk, and Viktor Antonovich Sadovnichy. "Mathematic Model for Prediction of Liver Fibrosis Progression Rate in Patients with Chronic Hepatitis C Based on Combination of Genomic Markers." Annals of the Russian academy of medical sciences 70, no. 6 (December 3, 2015): 651–61. http://dx.doi.org/10.15690/vramn548.

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Aim of study. To evaluate clinical significance of different combinations of gene polymorphisms IL-1b, IL-6, IL-10, TNF, HFE, TGF-b, ATR1, NOS3894, CYBA, AGT, MTHFR, FII, FV, FVII, FXIII, ITGA2, ITGB3, FBG, PAI and their prognostic value for prediction of liver fibrosis progression rate in patients with chronic hepatitis C (CHC).Subjects and methods: 118 patients with CHC were divided into «fast» and «slow» (fibrosis rate progression ≥0,13 and 0,13 fibrosis units/yr; n =64 and n =54) fibrosis groups. Gene polymorphisms were determined. Statistical analysis was performed using Statistica 10.Results. A allele (p =0,012) and genotype AA (p =0,024) of AGT G-6T gene, as well as T allele (p =0,013) and MT+TT genotypes (p =0,005) of AGT 235 M/T gene were significantly more common in «fast fibrosers» than in «slow fibrosers». Patients with genotype TT of CYBA 242 C/T had a higher fibrosis progression rate than patients with CC+CT genotype (p =0,02). Our analysis showed a protective effect of TT genotype of ITGA2 807 C/T on fibrosis progression rate (p =0,03). There was a trend (p 0,15) to higher fibrosis progression rate in patients with mutant alleles and genotypes of TGFb +915 G/C, FXIII 103 G/T, PAI -675 5G/4G genes. Other gene polymorphisms were not associated with enhanced liver fibrosis. To build a mathematical model for prediction of liver fibrosis progression rate we performed coding with scores for genotypes and virus genotype. Total score correlated with the fibrosis progression rate (R =0,39, p =0,000).Conclusion: Determination of genetic profile of the patient and virus genotype allows to predict the course of CHC.
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Jarčuška, Peter, Martin Janičko, Eduard Veselíny, Pavol Jarčuška, and Ľubomír Skladaný. "Circulating markers of liver fibrosis progression." Clinica Chimica Acta 411, no. 15-16 (August 2010): 1009–17. http://dx.doi.org/10.1016/j.cca.2010.04.009.

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Hagström, Hannes, Olof Elfwén, Rolf Hultcrantz, and Per Stål. "Steatohepatitis Is Not Associated with an Increased Risk for Fibrosis Progression in Nonalcoholic Fatty Liver Disease." Gastroenterology Research and Practice 2018 (July 2, 2018): 1–7. http://dx.doi.org/10.1155/2018/1942648.

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Introduction. Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease globally. The majority of NAFLD patients have fatty liver without inflammation (nonalcoholic fatty liver, NAFL), whereas a minority develop steatohepatitis (nonalcoholic steatohepatitis, NASH). Only NASH and not NAFL has been considered to increase the risk for fibrosis progression. The present study investigates risk factors for fibrosis progression in patients with NAFLD, and if fibrosis progression associates with subsequent mortality. Material and Methods. All patients with at least two liver biopsies more than a year apart at our hospital between 1971 and 2016 were identified. Data on plausible risk factors for fibrosis progression were collected. Biopsies were scored for the presence of NASH and fibrosis stage. Regression models were used to investigate the association between baseline NASH and fibrosis progression and fibrosis progression with future mortality. Results. 60 patients had undergone serial biopsies (median interval between biopsies 8.4 years, range 1–33 years), with 26 patients (43%) having fibrosis progression. We found no significant risk factors for progression of fibrosis except time between biopsies. Among patients with fibrosis progression, 54% had NAFL and 46% had NASH at baseline. There was a trend for an association between fibrosis progression per se and increased mortality (hazard ratio 2.83, 95% CI 1.0–8.1, p=0.05). Conclusions. In this study on NAFLD, baseline steatohepatitis was not associated with an increased risk for fibrosis progression. NAFLD patients without steatohepatitis may develop progressive fibrosis, and those with progressive fibrosis appear to have a higher mortality risk irrespective of baseline NASH status.
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Abenavoli, Ludovico, Christophe Corpechot, and Raoul Poupon. "Elastography in Hepatology." Canadian Journal of Gastroenterology 21, no. 12 (2007): 839–42. http://dx.doi.org/10.1155/2007/621489.

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A common characteristic of all chronic liver diseases is the occurrence and progression of fibrosis toward cirrhosis. Consequently, liver fibrosis assessment plays an important role in hepatology. Besides its importance for prognosis, determining the level of fibrosis reveals the natural history of the disease and the risk factors associated with its progression, to guide the antifibrotic action of different treatments. Currently, in clinical practice, there are three available methods for the evaluation of liver fibrosis: liver biopsy, which is still considered to be the ‘gold standard’; serological markers of fibrosis and their mathematical combination – suggested in recent years to be an alternative to liver biopsy – and, more recently, transient elastography (TE). TE is a new, simple and noninvasive method used to measure liver stiffness. This technique is based on the progressing speed of an elastic shear wave within the liver. Currently, there are only a few studies that have evaluated TE effectiveness in chronic liver diseases, mostly in patients infected with the hepatitis C virus. Further studies are needed in patients with chronic liver disease, to assess the effectiveness of the fibrosis treatment.
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Diamond, Tamir, and Nadia Ovchinsky. "Fontan-associated liver disease: Monitoring progression of liver fibrosis." Clinical Liver Disease 11, no. 1 (January 2018): 1–5. http://dx.doi.org/10.1002/cld.681.

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Koeckerling, David, Jeremy W. Tomlinson, and Jeremy F. Cobbold. "Fighting liver fat." Endocrine Connections 9, no. 7 (July 2020): R173—R186. http://dx.doi.org/10.1530/ec-20-0174.

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Non-alcoholic fatty liver disease is a chronic liver disease which is closely associated with components of the metabolic syndrome. Its high clinical burden results from the growing prevalence, inherent cardiometabolic risk and potential of progressing to cirrhosis. Patients with non-alcoholic fatty liver disease show variable rates of disease progression through a histological spectrum ranging from steatosis to steatohepatitis with or without fibrosis. The presence and severity of fibrosis are the most important prognostic factors in non-alcoholic fatty liver disease. This necessitates risk stratification of patients by fibrosis stage using combinations of non-invasive methods, such as composite scoring systems and/or transient elastography. A multidisciplinary approach to treatment is advised, centred on amelioration of cardiometabolic risk through lifestyle and pharmacological interventions. Despite the current lack of licensed, liver-targeted pharmacotherapy, several promising agents are undergoing late-phase clinical trials to complement standard management in patients with advanced disease. This review summarises the current concepts in diagnosis and disease progression of non-alcoholic liver disease, focusing on pragmatic approaches to risk assessment and management in both primary and secondary care settings.
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Nishimura, Norihisa, Davide De Battista, David R. McGivern, Ronald E. Engle, Ashley Tice, Rafaelle Fares-Gusmao, Juraj Kabat, et al. "Chitinase 3-like 1 is a profibrogenic factor overexpressed in the aging liver and in patients with liver cirrhosis." Proceedings of the National Academy of Sciences 118, no. 17 (April 22, 2021): e2019633118. http://dx.doi.org/10.1073/pnas.2019633118.

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Older age at the time of infection with hepatitis viruses is associated with an increased risk of liver fibrosis progression. We hypothesized that the pace of fibrosis progression may reflect changes in gene expression within the aging liver. We compared gene expression in liver specimens from 54 adult donors without evidence of fibrosis, including 36 over 40 y old and 18 between 18 and 40 y old. Chitinase 3-like 1 (CHI3L1), which encodes chitinase-like protein YKL-40/CHI3L1, was identified as the gene with the greatest age-dependent increase in expression in liver tissue. We investigated the cellular source of CHI3L1 in the liver and its function using liver tissue specimens and in vitro models. CHI3L1 expression was significantly higher in livers of patients with cirrhosis of diverse etiologies compared with controls represented by patients who underwent liver resection for hemangioma. The highest intrahepatic CHI3L1 expression was observed in cirrhosis due to hepatitis D virus, followed by hepatitis C virus, hepatitis B virus, and alcohol-induced cirrhosis. In situ hybridization of CHI3L1 messenger RNA (mRNA) identified hepatocytes as the major producers of CHI3L1 in normal liver and in cirrhotic tissue, wherein hepatocytes adjacent to fibrous septa showed higher CHI3L1 expression than did those in more distal areas. In vitro studies showed that recombinant CHI3L1 promotes proliferation and activation of primary human hepatic stellate cells (HSCs), the major drivers of liver fibrosis. These findings collectively demonstrate that CHI3L1 promotes liver fibrogenesis through a direct effect on HSCs and support a role for CHI3L1 in the increased susceptibility of aging livers to fibrosis progression.
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Chen, Wei, Xiaoning Wu, Xuzhen Yan, Anjian Xu, Aiting Yang, and Hong You. "Multitranscriptome analyses reveal prioritized genes specifically associated with liver fibrosis progression independent of etiology." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 6 (June 1, 2019): G744—G754. http://dx.doi.org/10.1152/ajpgi.00339.2018.

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Elimination or suppression of causative factors can raise the possibility of liver fibrosis regression. However, different injurious stimuli will give fibrosis from somewhat different etiologies, which, in turn, may hamper the discovery of liver fibrosis-specific therapeutic drugs. Therefore, the analogical cellular and molecular events shared by various etiology-evoked liver fibrosis should be clarified. Our present study systematically integrated five publicly available transcriptomic data sets regarding liver fibrosis with different etiologies from the Gene Expression Omnibus database and performed a series of bioinformatics analyses and experimental verifications. A total of 111 significantly upregulated and 16 downregulated genes were identified specific to liver fibrosis independent of any etiology. These genes were predominately enriched in some Kyoto Encyclopedia of Genes and Genomes pathways, including the “PI3K-AKT signaling pathway,” “Focal adhesion,” and “ECM-receptor interaction.” Subsequently, five prioritized liver fibrosis-specific genes, including COL4A2, THBS2, ITGAV, LAMB1, and PDGFRA, were screened. These genes were positively associated with each other and liver fibrosis progression. In addition, they could robustly separate all stages of samples in both training and validation data sets with diverse etiologies when they were regarded as observed variables applied to principal component analysis plots. Expressions of all five genes were confirmed in activated primary mouse hepatic stellate cells (HSCs) and transforming growth factor β1-treated LX-2 cells. Moreover, THBS2 protein was enhanced in liver fibrosis rodent models, which could promote HSC activation and proliferation and facilitate NOTCH1/JAG1 expression in HSCs. Overall, our current study may provide potential targets for liver fibrosis therapy and aid to a deeper understanding of the molecular underpinnings of liver fibrosis. NEW & NOTEWORTHY Prioritized liver fibrosis-specific genes THBS2, COL4A2, ITGAV, LAMB1, and PDGFRA were identified and significantly associated with liver fibrosis progression and could be combined to discriminate liver fibrosis stages regardless of any etiology. Among the identified prioritized liver fibrosis-specific targets, THBS2 protein was confirmed to be enhanced in liver fibrosis rodent models, which could promote hepatic stellate cell (HSC) activation and proliferation and facilitate NOTCH1/JAG1 expression in HSCs.
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He, Yuting, Chiang Huen Kang, Shuoyu Xu, Xiaoye Tuo, Scott Trasti, Dean C. S. Tai, Anju Mythreyi Raja, et al. "Toward surface quantification of liver fibrosis progression." Journal of Biomedical Optics 15, no. 5 (2010): 056007. http://dx.doi.org/10.1117/1.3490414.

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Rosenberg, William M. C. "Rating fibrosis progression in chronic liver diseases." Journal of Hepatology 38, no. 3 (March 2003): 357–60. http://dx.doi.org/10.1016/s0168-8278(03)00010-2.

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Dissertations / Theses on the topic "Liver fibrosis progression"

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Reichenbach, Marinkovic Vedrana. "Hepatic remodeling, serum biomarkers and prevention of fibrosis progression in liver disease." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/107757.

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Hepatic fibrosis is characterized by intense tissue remodeling. In this study, we assessed whether CO3-610, a new identified neoepitope, could be used as a surrogate biomarker of liver fibrosis and portal hypertension in CCl4-induced experimental fibrosis. Serum CO3-610 was measured by ELISA. Liver fibrosis was quantified by Sirius red staining. Serum hyaluronic acid (HA) was measured with a binding-protein assay. Gene expression of collagens I and III, MMP2 and MMP9, and tissue inhibitors of matrix metalloproteinase 1 and 2 was quantified by PCR. Hemodynamic measurements were taken in a subgroup of animals. A close direct relationship was found between serum CO3-610 and hepatic collagen content (r= 0.78; P<0.001), superior to that found for serum HA (r= 0.49; P<0.05). CO3-610 levels in rats with severe fibrosis (43.5±3.3 ng/mL, P<0.001) and cirrhosis (60.6±4.3 ng/mL, P<0.001) were significantly higher than those in control animals (26.6±1.3 ng/mL). Importantly, a highly significant relationship was found between serum CO3-610 and portal hypertension (r= 0.84; P<0.001). Liver MMP9 expression increased significantly in fibrotic animals but decreased to control levels in cirrhotic ones. Circulating CO3-610 behaves as a reliable indicator of hepatic remodeling and portal hypertension in experimental fibrosis. Therefore, this peptide could ultimately be a useful marker for the management of liver disease in patients. Endocannabinoids behave as antifibrogenic agents by interacting with cannabinoid CB2 receptors, whereas the apelin (AP) system acts as a proangiogenic and profibrogenic mediator in the liver. This study assessed the effect of long-term stimulation of CB2 receptors or AP receptor (APJ) blockade on fibrosis progression in rats under a non-discontinued fibrosis induction program. The study was performed in control and CCl4-treated rats for 13 weeks. Fibrosis-induced rats received a CB2 receptor agonist (AM1241) (1 mg/kg), an APJ antagonist (F13A) (75 μg/kg), or vehicle daily during the last 5 weeks of the CCl4 inhalation program. Mean arterial pressure (MAP), portal pressure (PP), hepatic collagen content, angiogenesis, cell infiltrate, and mRNA expression of a panel of fibrosis-related genes were measured in all animals. Fibrosis-induced rats showed increased hepatic collagen content, reduced MAP, PP, and increased expression of the assessed messengers in comparison with control rats. However, fibrotic rats treated with either AM1241 or F13A had reduced hepatic collagen content, improved MAP and PP, ameliorated cell viability, and reduced angiogenesis and cell infiltrate compared with untreated fibrotic rats. These results were associated with attenuated induction of PDGFRβ, α-SMA, MMPs, and TIMPs. CB2 receptor stimulation or APJ blockade prevents fibrosis progression in CCl4-treated rats. The mechanisms underlying these phenomena are coincident despite the marked dissimilarities between the CB2 and APJ signaling pathways, thus opening new avenues for preventing fibrosis progression in liver diseases. PDGF is the most potent stimulus for proliferation and migration of stellate cells. PDGF receptor β expression is an important phenotypic change in myofibroblastic cells that mediates proliferation and chemotaxis. Here we analyzed the relationship between PDGFRβ expression, hemodynamic deterioration, and fibrosis. Thereafter, we investigated the effects produced by an adenovirus encoding a dominant-negative soluble PDGFRβ (sPDGFRβ) on hemodynamic parameters, PDGFRβ signaling pathway, and fibrosis. Hemodynamics, PDGFRβ mRNA expression, and hepatic collagen were assessed in controls and fibrosic/cirrhotic rats. Next, 30 fibrotic rats were randomized into three groups receiving iv saline and an adenovirus encoding for sPDGFRβ or β-galactosidase. After 7days, hemodynamics, serum sPDGFRβ, and hepatic collagen were measured. CCl4-treated animals for 18weeks showed a significantly higher increase in PDGFRβ mRNA compared to those treated for 13weeks and control rats. In CCl4-treated rats, the fibrous tissue area ranged from moderate to severe fibrosis. A direct relationship between the degree of fibrosis, hemodynamic changes, and PDGFRβ expression was observed. Fibrotic rats transduced with the adenovirus encoding sPDGFRβ showed increased MAP, decreased PP, lower activation of the PDGFRβ signaling pathway, and reduced hepatic collagen than fibrotic rats receiving β-gal or saline. PDGFRβ activation closely correlates with hemodynamic disorders and increased fibrosis in CCl4-treated rats. Adenoviral dominant negative soluble PDGFRβ improved fibrosis. As a result, the hemodynamic abnormalities were ameliorated. Cirrhotic patients have altered host-defense response mechanisms. Here we assessed whether impaired expression of CB2 receptor in monocytic cells of cirrhotic patients could be involved in the pathogenesis of this phenomenon. CB2 mRNA and protein expression was assessed in a differentiated human monocytic cell line (U937) stimulated with endotoxin (LPS). A PCR array of 86 different genes was assessed in U937 cells treated with LPS. A migration assay towards endocannabinoids or the CB2 antagonist, SR144528, was performed in U937 cells exposed to LPS. Finally, CB1 and CB2 mRNA expression were measured in monocytes and macrophages of cirrhotic patients with or without spontaneous bacterial peritonitis. LPS reduced CB2 expression in human monocytes. Endocannabinoids increased the migratory activity of U937 cells, which was reverted when the experiments were performed in the presence of LPS. Transcriptional profiling showed marked upregulation of 9 genes related to proinflammatory signaling. However, only two genes encoding for CB1 and CB2 were reduced in LPS-treated cells. Circulating monocytes of cirrhotic patients showed a significantly diminished mRNA expression of CB1 and CB2. Markedly low CB1 and CB2 mRNA levels were found in peritoneal macrophages of cirrhotic patients with ascites, being almost suppressed when analyzed in patients with peritonitis. LPS reduces CB2 expression in human monocytes resulting in depressed chemotactic activity and therefore impaired host defense response of these cells.
La característica más destacable de la fibrosis es la desregulación de la ME. El equilibrio que existe entre la síntesis y la degradación de la ME en un hígado normal se pierde, y como consecuencia se favorece la síntesis y acumulación de fibras de colágeno, el cual provoca la distorsión de la arquitectura del parénquima y de la red vascular hepática. El CO3-610 es un producto de degradación del colágeno III que ha mostrado estar correlacionado significativamente con el aumento de la cantidad de colágeno y progresión de la fibrosis. Los valores máximos de CO3-610 se han encontrado ratas cirróticas. El resultado más importante es que el CO3-610 ha mostrado tener una estrecha correlación con los valores de presión portal. Existe un gran interés en investigar y desarrollar terapias dirigidas a la prevención de la progresión de la fibrosis. Los endocannabinoides son moléculas lipídicas que participan en un amplio rango de procesos fisiológicos. Los efectos son mediados por dos tipos de receptores, el CB1 y el CB2. El sistema de la apelina es otro sistema endógeno que ha despertado mucho interés en los últimos años. La apelina es el único ligando conocido para el receptor APJ. El tratamiento con AM1241, un agonista selectivo de CB2 y F13A, un antagonista de APJ mejoró la función hepática, la hemodinámica sistémica y portal, y provocó una reducción significativa del grado de fibrosis hepática. Ambos tratamientos produjeron una disminución del infiltrado inflamatorio, angiogénesis y del grado de apoptosis en el parénquima hepático. El análisis de la expresión del mRNA de varios genes importantes implicados en el proceso fibrogénico, reveló que el tratamiento tanto con AM1241 como con F13A, producían una disminución de la expresión del PDGFRβ, del αSMA y de genes de remodelado tisular. La inhibición parcial de la vía de PDGF mediante la administración de un dominante negativo para la fracción soluble del receptor β de PDGF, ha demostrado que mejora la hemodinámica sistémica y la presión portal además de mejorar el grado de fibrosis. Por último, los pacientes cirróticos con ascitis tienen una mayor probabilidad de sufrir infecciones (peritonitis bacteriana espontánea, PBE). Se ha observado que estos pacientes tienen una menor expresión de CB2. In vitro se han realizado experimentos con células monocíticas (U937) y se ha observado que el LPS disminuye drásticamente la expresión de CB2 al igual que afecta a la capacidad de migración de estas células. En conjunto, se puede concluir que la evaluación de la fibrosis hepática es una herramienta muy importante para el diagnostico de la enfermedad hepática y que éste puede mejorarse a través del uso de biomarcadores no invasivos que correlacionen con la hemodinámica y el grado de fibrosis hepática. La prevención de la progresión de la fibrosis a través de fármacos o bien actuando sobre genes clave involucrados en la fibrogénesis son posibles dianas terapéuticas. Finalmente, es posible mejorar la calidad de vida de los pacientes cirróticos con ascitis con infección por PBE mediante terapias que involucren los receptores de cannabinoides CB2.
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Hui, Chee-kin, and 許志堅. "Chronic hepatitis C infection: diagnosis, fibrosis progression and interferon therapy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29756972.

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Jobara, Kanta. "Whey-hydrolyzed peptide-enriched immunomodulating diet prevents progression of liver cirrhosis in rats." Kyoto University, 2014. http://hdl.handle.net/2433/189665.

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Trepo, Eric. "Role of genetic factors in the progression of fibrosis in alcoholic liver disease and chronic hepatitis C." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209659.

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La maladie alcoolique du foie (MAF) et l’hépatite C chronique (HCC) sont les causes les plus fréquentes de cirrhose, carcinome hépatocellulaire (CHC) et transplantation hépatique dans les pays industrialisés. La fibrose hépatique est le stigmate lésionnel de la progression de la maladie vers la cirrhose comme dans toutes les hépatopathies chroniques. Certains facteurs de risque cliniques environnementaux ont été identifiés. Toutefois, ils n’expliquent pas l’extrême variabilité individuelle de la progression de la fibrose. L’influence ethnique à développer une maladie plus sévère ainsi que les études de concordance des jumeaux mono- et di-zygotiques sur la prévalence de la cirrhose alcoolique ont suggéré l’existence de facteurs génétiques associés. Les nombreuses études de gènes candidats réalisées n’ont identifié que très peu de variants associés de manière reproductible. Pour l’HCC par exemple, le score de risque de cirrhose ou « CRS » a montré sa capacité à prédire une fibrose avancée dans diverses cohortes caucasiennes. Récemment, une étude d’association pangénomique (GWAS) dans la stéatohépatopathie non-alcoolique (NAFLD) a mis en évidence un singleton (single nucleotide polymorphism [SNP]) particulier (rs738409 C>G) dans le gène PNPLA3. Ce dernier s’est révélé être, dans diverses études, le SNP ayant l’impact le plus robuste et le plus reproductible dans cette maladie. Par ailleurs, ce même variant a également été significativement associé à la cirrhose alcoolique chez les hispaniques.

Les travaux réalisés dans le cadre de cette thèse ont permis de montrer que :

1) Le CRS avait la capacité de prédire la progression de la fibrose chez des patients caucasiens ayant une HCC dans 2 cohortes européennes indépendantes.

2) Par ailleurs, dans la MAF, nous avons répliqué chez des patients caucasiens l’association entre le SNP rs738409 dans le gène PNPLA3 et la cirrhose. Nous avons également montré pour la première fois, que l’expression de PNPLA3 était significativement diminuée chez les patients avec une fibrose plus avancée. De plus, nous avons observé dans 2 cohortes européennes que rs738409 était également associé à la prévalence du CHC.

3) Enfin, nous avons également mis en évidence l’impact de ce même SNP sur la stéatose hépatique et la fibrose dans l’HCC sans toutefois qu’il influence la réponse à la thérapie antivirale dans 3 cohortes caucasiennes indépendantes.

Ainsi de manière remarquable, un même SNP (rs738409) apparait associé à des lésions hépatiques sévères dans les trois pathologies hépatiques chroniques les plus fréquentes (la MAF, l’HCC et la NAFLD). Ceci suggère des voies pathogéniques communes de la fibrogénèse hépatique. Par ailleurs, ces travaux soulignent indirectement que les GWAS ont la capacité d’ouvrir de nouvelles voies physiopathologiques et d’identifier de nouveaux variants, gènes ou région génétiques capables de constituer de nouveaux biomarqueurs et cibles thérapeutiques dans l’HCC et la MAF.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished

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MacFarlane, David Peter. "Factors determining the progression of nonalcoholic fatty liver disease : the role of abnormal fatty acid and glucocorticoid metabolism." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5914.

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Obesity and insulin resistance are associated with a constellation of features including hypertension, dyslipidaemia, type 2 diabetes, and premature cardiovascular disease, collectively termed the metabolic syndrome. Non-alcoholic fatty liver disease (NAFLD) represents the hepatic component of this syndrome, incorporating a spectrum of liver disease with increasing morbidity and mortality, from simple steatosis, to non-alcoholic steatohepatitis (or NASH), fibrosis, cirrhosis and ultimately hepatocellular carcinoma. However, factors influencing this progression are incompletely understood. In this thesis I sought to investigate pathways which promote hepatic inflammation and fibrosis by studying two contrasting dietary models of NAFLD in mice in which the risk of hepatic inflammation, insulin resistance and fibrosis differ; namely the methionine and choline deficient diet (MCDD) which induces steatohepatitis, hepatic insulin resistance, and weight loss, and the choline deficient diet (CDD) which may be protected from insulin resistance, and leads to steatosis without inflammation or weight loss. I investigated the possible molecular mechanisms underlying these differences, and whether they influenced progression to hepatic fibrosis induced by carbon tetrachloride (CCl4).
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Singh, Harnoor. "YKL-40 as a non-invasive serum marker in assessment of rapid fibrosis progression post-orthotopic liver transplantation." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12629.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Liver biopsy has been considered the gold standard method to assess the progression of fibrosis in chronic hepatitis C viral infection. Despite its prevalent use, significant complications along with patient discomfort are often reported. A reliable, non-invasive method to assess rapid fibrosis progression in patients with HCV infection must be determined. This study involved 57 subjects that underwent liver transplantation due to end stage liver disease as a result of chronic HCV infection. Serum samples were collected from all subjects at time of biopsy. Measurement of YKL-40 was performed using ELISA assays. Serum samples collected for all subjects at time of biopsy had a total YKL-40 concentration range from 38-1442 ng/mL with a mean of 228.74 ng/mL and a standard deviation of 271.26 ng/mL. The median YKL-40 concentration was 128 ng/mL. Serum YKL-40 is a reliable marker of rapid fibrosis progression and can be used in combination with other markers to accurately predict rapid fibrosis progression in HCV infected patients post orthotopic liver transplantation.
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Azar, Fida. "Rôle de la protéine ADAMTS12 dans la progression des maladies hépatiques chroniques." Thesis, Rennes 1, 2021. http://www.theses.fr/2021REN1B001.

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Les maladies chroniques du foie (CLD) sont associées au développement de la fibrose et caractérisées par un dépôt excessif de matrice extracellulaire (MEC), conduisant à une cirrhose et au carcinome hépatocellulaire (CHC). Lors d'une lésion hépatique, les hépatocytes endommagés déclenchent une réponse inflammatoire qui active les cellules étoilées hépatiques (CEH). Une fois activées, ces cellules se transdifférencient en myofibroblastes et produisent des composants de la MEC parmi lesquels les protéines de la famille des adamalysines (ADAM et ADAMTS). Quand le tissu est cicatrisé, la sénescence et d'autres mécanismes contribuent à la clairance ou à la réversion des CEHs. Récemment, nous avons identifié ADAMTS12 comme une adamalysine potentiellement impliquée dans la progression des CLDs. L’objectif de cette étude était d’explorer les fonctions cellulaires d'ADAMTS12 dans les CEH, et son rôle dans les CLDs. Chez les patients atteints de CHC, nous avons montré que l'expression d'ADAMTS12 est associée à l'agressivité et à la récidive des tumeurs. ADAMTS12 est exprimée par les CEH et par la lignée cellulaire LX-2 dérivée des CEH, mais pas par les hépatocytes. La fibrose induite par le CCl4 est exacerbée dans les souris ADAMTS12-/-. L’analyse transcriptomique de la lignée de CEH LX-2 montre une diminution de l'expression de PAI-I, un gène cible du TGF-β et un marqueur et médiateur de la sénescence lorsque l’expression d‘ADAMTS12 est réprimée par ARN-interférence (siADAMTS12). L'activation du TGF-β à partir de son précurseur LAP-TGF-β n’est pas affectée dans ce modèle mais on observe une diminution de la phosphorylation de smad2, suggérant que la répression du gène ADAMTS12 entraîne une inhibition de la voie SMAD de réponse au TGF-β. De plus, l’invalidation d'ADAMTS12 diminue la sénescence dans les LX-2. Par ailleurs, les données RNA-seq ont également montré une augmentation des gènes impliqués dans l'organisation du cil primaire dans les cellules siADAMTS12. L’immuno-détection d’une protéine du cil, ARL13b, a montré une augmentation du nombre de cils et une diminution de leur longueur dans les cellules siADAMTS12. De plus, l’absence d’ADAMTS12 dans LX-2 augmente le nombre de cellules en phase S. Nos résultats suggèrent qu'en absence d'ADAMTS12, les CEH échappent à la sénescence, ce qui, dans l'ensemble du contexte tissulaire, les rendrait compétentes pour la prolifération et la différenciation en myofibroblastes
Chronic Liver Diseases (CLDs) are associated with the development of fibrosis and characterized by excessive deposit of extracellular matrix (ECM), leading to cirrhosis and increasing risk of hepatocellular carcinoma (HCC). During liver injury, an inflammatory response activates the hepatic stellate cells (HSCs), whose function in normal liver is to store Vitamin A. Once activated these cells lose their vitamin A and transdifferentiate into myofibroblasts which produce ECM components among them proteins of the adamalysin (ADAM and ADAMTS) family. This family of metalloproteinases is implicated in several functions in the normal and pathological liver, and several members contribute to ECM remodeling in liver pathologies. Once the injury subsides, senescence and other mechanisms contribute to HSC clearance or reversion. Recently, we identified ADAMTS12 as an adamalysin potentially involved in CLD progression. The purpose of this study was to decipher the cellular functions of ADAMTS12 in HSCs and its role in CLDs. We found that in HCC patients, the expression of ADAMTS12 is associated with aggressiveness and recurrence. ADAMTS12 was expressed by activated HSCs as well as the HSC-derived LX-2 cell line, but not by the hepatocytes. CCl4-induced fibrosis was exacerbated in ADAMTS12 -/- mice. Transcriptomic analysis of the HSC-derived LX-2 cell line showed a down-regulation of the expression of PAI-1, a gene target of TGF-β and a marker and mediator of senescence upon ADAMTS12 silencing (siADAMTS12). TGF- β activation from its precursor was not affected in this model, although the phosphorylation of smad2 was decreased, suggesting that ADAMTS12 silencing leads to an inhibition of the SMAD-dependent TGF-β signaling pathway. In addition, silencing of ADAMTS12 decreased senescence in LX-2 cell line. Furthermore, RNA-seq data showed an up-regulation in genes implicated in the organization of primary cilium upon ADAMTS12 silencing. Immunodetection of the protein ARL13b, a primary cilium component, showed an increase in the number of cilia and a decrease in their length in siADAMTS12 cells. Additionally, ADAMTS12 silencing in LX-2 increased the G1 to S transition. Our results suggest that in the absence of ADAMTS12, HSCs escape senescence, which render them competent for myofibroblast differentiation and proliferation
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Thorpe, Julia. "Assessing the impact of antiretroviral treatment interruption on progression of liver fibrosis in adults co-infected with HIV and hepatitus C." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95226.

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Objective: Despite the evidence that antiretroviral treatment (ART) interruption increases the risk of various negative outcomes, it is still likely that HIV/hepatitis C (HCV) co-infected patients will discontinue ART for several reasons. The impact of interruption on liver fibrosis progression in co-infected adults was examined, using the aspartate aminotransferase-to-platelet ratio index (APRI) as a surrogate marker of liver fibrosis. Method: Time-dependent Cox regression, as well as inverse probability-of-treatment weighting (IPTW) in a marginal structural model, were used to evaluate the association of baseline and time-varying covariates with developing significant fibrosis. Results: After accounting for potential confounders, such as HIV viral load and CD4+ T cell count, the hazard ratio for ART interruption was 2.52 (1.20-5.28). Use of IPTW resulted in a similar estimate of effect, suggesting that mediation by time-varying confounders was negligible. Conclusions: ART interruption was independently associated with an increased risk of liver fibrosis progression in HIV/HCV co-infected patients.
Objectif: Certains patients coinfectés par le VIH et l'hépatite C interrompent leur traitement antirétroviral (TRT) pour des raisons variées, bien que cela augmente les risques de plusieurs effets indésirables. L'impact de l'interruption du traitement sur la progression de fibrose du foie chez des adultes coinfectés a donc été évalué grâce à l'utilisation du score APRI comme marqueur de fibrose du foie. Méthode: Un modèle Cox ainsi qu'un modèle marginal avec pondération par l'inverse de la probabilité de traitement ont été utilisés. Résultats: Après ajustement, le rapport de risque pour l'interruption du TRT était de 2.52 (1.20-5.28). Un effet similaire a été mesuré lorsque la pondération par l'inverse de la probabilité de traitement a été utilisée, ce qui suggère que l'effet des variables variant avec le temps était négligeable. Conclusions: L'interruption du TRT est indépendamment associée avec un risque accru de la progression de fibrose du foie chez les patients coinfectés avec le VIH et l'hépatite C.
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MARABITA, FRANCESCO. "Single Nucleotide Polymorphisms and circulating microRNAs for monitoring HCV disease progression: an integrated approach." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/29993.

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Chronic Hepatitis C Virus (HCV) infection is associated with severe complications such as liver cirrhosis and hepatocellular carcinoma (HCC). For HCV infection, there is a crucial need for novel, preferably non‐invasive tests that could be used to improve the diagnosis and the management programs for patients at high risk of developing severe liver complications, such as cirrhosis and HCC. Classical biochemical markers to follow disease progression show limited potential mainly for invasiveness or little specificity and sensitivity, especially for HCC. The goal of this work was to discover useful biomarkers of disease progression in the setting of chronic HCV infection. In the first part, a Genome Wide Association Study was carried out to study the genetic variability influencing the natural history of HCV infection. A cohort of patients was genotyped and disease stage was evaluated through a liver biopsy before any antiviral treatment. Although no hits reached a genome-wide significance level, candidate regions showing suggestive association were identified. In particular, the gene region containing the GADD45G gene resulted of particular interest, given its role in cell biology. Conversely, the analysis of covariates revealed that they had a profound impact on the progression of the liver disease. Indeed, the age at infection had a marked effect on fibrosis progression (p < 2E‐16), suggesting that this is the major explanatory variable in our cohort. Male gender (p < 0.05) and HCV genotype 3 (p < 0.01) were also associated to faster fibrosis progression. The second part of this work focused on the use of circulating microRNA as blood-based biomarker of disease status. We investigated whether specific serum miRNA signatures may be detected in the serum of patients with chronic HCV infection at different stages of liver disease. Individual sera from healthy controls, patients with chronic hepatitis, liver cirrhosis or HCC were tested by high‐throughput qPCR to profile the expression of the whole miRNome. A solid normalization strategy was applied to reduce variability, and 22 miRNAs were considered differentially represented among the four classes (p<0.05 after multiple testing correction) The levels of miR‐122 and miR‐885‐5p specifically and consistently increased in patients with HCV infection compared to healthy controls or patients with Cronh’s disease (p<0.001). miR‐122 concentration changed significantly among groups with different alanine aminotransferase (ALT) activity (p<0.001), showing a positive trend. In summary, serum levels of miR‐122 and miR‐885‐5p were significantly elevated in patients with HCV‐associated liver pathologies. Our data show the potential use of serum miRNA as novel biomarker in the setting of chronic HCV infection.
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Murata, Toru. "Inhibitory effect of Y-27632,a ROCK inhibitor,on progression of rat liver fibrosis in association with inactivation of hepatic stellate cells." Kyoto University, 2002. http://hdl.handle.net/2433/149343.

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Books on the topic "Liver fibrosis progression"

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Snell, Jamey, and Thomas J. Mancuso. Cystic Fibrosis. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0023.

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Cystic fibrosis (CF) is an inherited, autosomal recessive, multisystem disease. Dysfunction of the cystic fibrosis transmembrane conductance regulator protein (CFTR) in epithelial cells is the primary defect in CF. Defects in CFTR are the cause for lung disease, exocrine pancreatic insufficiency and failure, male infertility, and liver disease. CF can present with a variety of respiratory and gastrointestinal signs, including meconium ileus in the newborn period, hypernatremic dehydration, pulmonary insufficiency, nasal polyps, and insulin-dependent diabetes mellitus. As affected children grow, dysfunction in CFTR leads to chronic and progressive lung disease, characterized by suppurative infection and the development of bronchiectasis. CFTR dysfunction also affects exocrine function, leading to pancreatic insufficiency, malabsorption, and growth failure. In the past, history and physical exam with sweat chloride testing were the cornerstones of diagnosis. Diagnosis is now made with the newborn screening test for immunoreactive trypsinogen.
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Kriemler, Susi. Exercise, physical activity, and cystic fibrosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0033.

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Cystic fibrosis (CF) is the most common genetic autosomal recessive disease of the Caucasian race, generally leading to death in early adulthood.1 The frequency of the gene carrier (heterozygote) is 1:20–25 in Caucasian populations, 1:2000 in African-Americans, and practically non-existent in Asian populations. The disease occurs in about 1 in every 2500 life births of the white population. Mean survival has risen from 8.4 years in 1969 to 32 years in 2000 due to improvements in treatment. The genetic defect causes a pathological electrolyte transport through the cell membranes by a defective chloride channel membrane transport protein [cystic fibrosis transmembrane conductance regulator (CFTR)]. With respect to the function, this affects mainly the exocrine glands of secretory cells, sinuses, lungs, pancreas, liver, and the reproductive tract of the human body leading to a highly viscous, water-depleted secretion. The secretion cannot leave the glands and in consequence causes local inflammation and destruction of various organs. The main symptoms include chronic inflammatory pulmonary disease with a progressive loss of lung function, exocrine and sometimes endocrine pancreas insufficiency, and an excessive salt loss through the sweat glands.1 A summary of the signs and symptoms of CF will be given with a special emphasis on the effect of exercise performance and capacity.
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Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.

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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of drug-induced CTIN largely depends on the history of exposure to a nephrotoxic drug. Clinical investigations may show modest elevation in serum creatinine, evidence of tubular dysfunction (e.g. renal tubular acidosis), or Fanconi syndrome (i.e. aminoaciduria, glycosuria, hypophosphataemia, and hypouricaemia). Urinalysis may be normal or show low-grade proteinuria (< 1.5 g/day) and/or pyuria. Diagnosis depends on renal biopsy, which reveals variable cellular infiltration of the interstitium, tubular atrophy, and fibrosis. Analgesic nephropathy is possibly still the most common category of CTIN worldwide. The amount of phenacetin-acetaminophen combination required to cause CTIN has been estimated to be at least 2–3 kg over many years. Lithium-induced CTIN occurs in a small subset of patients receiving long-term lithium therapy, who have had repeated episodes of lithium toxicity, with high serum drug levels. CTIN induced by ciclosporin or tacrolimus is common among patients receiving kidney, heart, liver, and pancreas transplants. The mechanism appears to be dependent largely on the potent vasoconstrictive effects of these drugs. The recognition of a potential association between a patient’s renal disease and exposure to a drug is crucial, because, unlike many other forms of renal disease, drug-induced CTIN can be prevented and even reversed, by avoiding additional drug exposure.
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Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.

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AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.
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Book chapters on the topic "Liver fibrosis progression"

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Syn, Wing-Kin, and Anna Mae Diehl. "Fibrosis progression." In Clinical Dilemmas in Non-Alcoholic Fatty Liver Disease, 59–71. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924938.ch8.

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Arthur, Michael J. P. "Mechanisms of Progression and Regression of Liver Fibrosis." In Liver Cirrhosis, 1–9. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-68343-8_1.

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Mueller, Sebastian. "Role of Sinusoidal Pressure and Arterialization in Driving Fibrosis Progression." In Liver Elastography, 671–83. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-40542-7_57.

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Vilaseca, Marina, and Jordi Gracia-Sancho. "Drugs to Modify Liver Fibrosis Progression and Regression." In Portal Hypertension VII, 201–18. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08552-9_18.

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Husain, Hadiya, and Riaz Ahmad. "Pathogenesis, Molecular Mechanisms of Progression, and Therapeutic Targets of Liver Fibrosis: An Update." In Clinical Biochemistry and Drug Development, 189–204. Includes bibliographical references and index.: Apple Academic Press, 2020. http://dx.doi.org/10.1201/9780367821470-14.

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Shah, Sharad, Prasanna Shah, and Khyati Shah. "Reversing of Fibrosis." In Preventive Measures for Cirrhosis of Liver and its Progression, 147. Jaypee Brothers Medical Publishers (P) Ltd., 2016. http://dx.doi.org/10.5005/jp/books/12878_5.

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Nayeb-Hashemi, Hamed, and Chinweike Ukomadu. "Cirrhosis." In The Brigham Intensive Review of Internal Medicine, 768–76. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199358274.003.0074.

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Cirrhosis is defined as a diffuse process characterized by fibrosis and conversion of normal architecture to structurally abnormal nodules. These regenerative nodules lack normal lobular organization and are surrounded by fibrous tissue. The word “cirrhosis” derives from Greek meaning tawny (the orange-yellow color of the diseased liver). René Laennec in 1819 coined the name cirrhosis to describe livers so diseased. The progression of liver injury to cirrhosis may occur over weeks to years. The chief complications are ascites, encephalopathy, and variceal bleeding.
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Hamoud, Shadi. "Role of the Enzyme Heparanase in the Development of Fatty Liver." In Non-alcoholic Fatty Liver Disease - New Insight and Glance Into Disease Pathogenesis [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.107530.

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Increasing evidence implicates the enzyme Heparanase in the development and progression of liver steatosis and fibrosis, where high heparanase expression was demonstrated. Morever, inhibition of heparanase activity significantly attenuated the development of fatty liver in animal models. Non-alcoholic fatty liver disease is the most common liver disease in the western world, with the natural course of a chronic progressive condition that is expected to worsen with time. Potential complications of the disease are steatohepatitis, liver fibrosis, liver cirrhosis and even liver malignancies, such as hepato-cellular carcinoma. As such, non-alcoholic fatty liver disease is considered a leading etiology for liver transplantation in the western world. No effective treatment for fatty liver is available so far, and seeking effective treatment strategies is of great importance. The aim of this chapter is to shed light on the knowledge regarding the involvement of Heparanase in the development and progression of fatty liver, opening the opportunity for future research of potential therapeutic options for treating this common liver pathology.
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Anstee, Quentin M., and Christopher P. Day. "Nonalcoholic fatty liver disease." In Oxford Textbook of Medicine, edited by Jack Satsangi, 3147–55. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0328.

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Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder in the developed world, affecting 20 to 30% of Western adults. Nonalcoholic liver disease occurs with a range of severity from simple steatosis through nonalcoholic steatohepatitis (NASH) to fatty fibrosis and, ultimately, cirrhosis. The condition is a manifestation of the metabolic syndrome, strongly associated with obesity, insulin resistance, and dyslipidaemia. Dietary and genetic factors appear to determine susceptibility to the disease and its progression. In most patients, the condition is discovered incidentally when abnormal values of serum liver-related liver tests are reported. The diagnosis is usually one of exclusion. Liver biopsy is not always required but, in the absence of well-validated noninvasive biomarkers, remains the only way to detect steatohepatitis and accurately stage fibrosis of intermediate severity. However, biopsy is not practical in all cases and so a staged approach to patient assessment and risk stratification is advised. Treatment is directed at components of the metabolic syndrome: weight loss through diet and exercise has been shown to ameliorate disease. A range of novel pharmacological drug treatments are under evaluation.
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Arthur, Michael J. P. "Role of Tissue Inhibitors of Metalloproteinases (TIMPs) in the Progression and Regression of Liver Fibrosis." In Extracellular Matrix and the Liver, 347–59. Elsevier, 2003. http://dx.doi.org/10.1016/b978-012525251-5/50020-8.

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Conference papers on the topic "Liver fibrosis progression"

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Lara, James, Yury Khudyakov, Marina Berenguer, F. Xavier Lopez-Labrador, and Fernando Gonzalez Candelas. "Hepatitis C virus genetic association to rate of liver fibrosis progression." In 2013 IEEE 3rd International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2013. http://dx.doi.org/10.1109/iccabs.2013.6629225.

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Evely, R. S., F. E. Preston, D. R. Triger, C. R. M. Hay, M. C. Greves, and J. C. E. Underwood. "TYPE III PRO-COLLAGEN PEPTIDE IN LIVER DISEASE IN HAEMOPHILIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644022.

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During the past 10 years we have carried out liver biopsies on haemophiliacs with biochemical evidence of chronic liver disease (CLD). To date 44 biopsies have been obtained from 35 patients. Histological diagnoses are Chronic Persistent Hepatitis (CPH) 24, Chronic Aggressive Hepatitis (CAH) 11 and Cirrhosis 9. Serial biopsies indicate that progressive liver disease is now a serious problem in haemophilia. Liver biopsy is not without risk and therefore it is important to identify factors which may be of value in predicting the nature of the liver disease or its progression. Since intra-hepatic fibrosis is a feature of CLD we measured Type III amino terminal propeptide of pro-collagen (PC III) by radio-immunoassay on samples taken within a mean of 4.8 months of the liver biopsy. A normal range was established as 4.3 - 15.7ng/ml on healthy subjects (median 7.0). Median values and ranges for patients with CPH (N=13), CAH (N=5) and cirrhosis (N=5) were 8 (5.4 - 23.4), 14.2 (7.2 - 19.8) and 14.2 (11.2 - 23.0)ng/ml respectively. Although pro-collagen III values tended to be higher in progressive liver disease (CAH and cirrhosis) this did not reach statistical significance. It would, therefore, appear that unlike serum IgG, pro-collagen III will not be a valuable predictor of progressive liver disease in haemophilia. A larger study is necessary to clarify this.
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Lederer, P., M. Roderfeld, DC Kroy, E. Roeb, A. Geier, and HM Hermanns. "Progression of fatty liver disease to steatohepatitis and liver fibrosis is associated with altered Oncostatin M type I and type II receptor expression." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677170.

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Susanto, Hendra, Fahdina Rufiandita, Gufron Alifi, Ahmad Taufiq, Wira Eka Putra, Ainul Mardiah, Dianvita Nur Fadhilah, Naily Salma Abadi, Novi Sanita Putri, and Siti Bachrotus Recha Nur Fa'ida. "Anti-inflammatory properties green material Moringa oleifera leaf powder (MOLP) on the progression of hepatocellular carcinoma-associated liver fibrosis." In INTERNATIONAL CONFERENCE ON LIFE SCIENCES AND TECHNOLOGY (ICoLiST 2020). AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0052574.

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Hennings, J., A. Hübbers, C. Penners, D. Lambertz, T. Otto, C. Trautwein, R. Sonntag, and C. Liedtke. "Cyclin E1 and Cdk2 in Hepatic Stellate Cells are critical for initiation and progression of liver fibrosis and cancer." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1722038.

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Sreedhar, Hari, Mamta Pant, Nemencio R. Ronquillo, Bennett Davidson, Peter Nguyen, Rohini Chennuri, Jacqueline Choi, et al. "Investigating the biochemical progression of liver disease through fibrosis, cirrhosis, dysplasia, and hepatocellular carcinoma using Fourier transform infrared spectroscopic imaging." In SPIE BiOS, edited by Anita Mahadevan-Jansen and Wolfgang Petrich. SPIE, 2014. http://dx.doi.org/10.1117/12.2040408.

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Hennings, J., A. Hübbers, C. Penners, D. Lambertz, T. Otto, C. Trautwein, R. Sonntag, and C. Liedtke. "Expression of Cyclin E1 and Cdk2 in Hepatic Stellate Cells is critical for initiation and progression of liver fibrosis in mice." In DGVS Digital: BEST OF DGVS. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1716094.

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Zhang, Zihao, Sheng Tong, and Gang Bao. "Development of Nanoparticle Probes for In Vivo Imaging of Atherosclerotic Plaques." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80149.

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Atherosclerosis, the formation of fatty plaques in the arterial lumen, is mediated by inflammatory macrophage infiltration in the lesion and ingestion of low-density lipoprotein (LDL), forming foam cells. Its progression will likely form a large necrotic core and fibrotic cap surface defects. The resulting intraplaque hemorrhage causes red blood cell infiltration and hemoglobin abundance, which oxidizes LDL to form cholesterol crystal aggregates (1). Hemorrhagic plaques could rupture and form artery-blocking emboli. Thus, it is critical to develop a tool to detect and locate unstable hemorrhagic plaques in live specimens.
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Reports on the topic "Liver fibrosis progression"

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Liu, Xiaopei, Dan Liu, and Cong’e Tan. Gut microbiome-based machine learning for diagnostic prediction of liver fibrosis and cirrhosis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0133.

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Review question / Objective: The invasive liver biopsy is the gold standard for the diagnosis of liver cirrhosis. Other non-invasive diagnostic approaches, have been used as alternatives to liver biopsy, however, these methods cannot identify the pathological grade of the lesion. Recently, studies have shown that gut microbiome-based machine learning can be used as a non-invasive diagnostic approach for liver cirrhosis or fibrosis, while it lacks evidence-based support. Therefore, we performed this systematic review and meta-analysis to evaluate its predictive diagnostic value in liver cirrhosis or fibrosis. Condition being studied: Liver fibrosis and cirrhosis. Liver fibrosis refers to excessive deposition of liver fibrous tissue caused by various pathogenic factors, such as hepatitis virus, alcohol, and drug-induced chemical injury. Continuous progression of liver fibrosis can lead to liver cirrhosis.
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Chen, Tiantian. The effect of vitamin D supplementation on the progression of fibrosis in patients with chronic liver disease: a protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0054.

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