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Bibliographies thématiques / Non Alcholic Steatohepatitis PDGF

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Littérature scientifique sur le sujet « Non Alcholic Steatohepatitis PDGF »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Non Alcholic Steatohepatitis PDGF"

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Desai, Tusar K. "Phlebotomy reduces transaminase levels in patients with non-alcholic steatohepatitis." Gastroenterology 118, no. 4 (2000): A975. http://dx.doi.org/10.1016/s0016-5085(00)86044-8.

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Granieri, C., S. Bagaglio, E. Loggi, et al. "T-47 High prevalence of occult hepatitis C virus infection in non alcholic steatohepatitis and cryptogenetic liver diseases." Digestive and Liver Disease 43 (February 2011): S91—S92. http://dx.doi.org/10.1016/s1590-8658(11)60083-2.

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El Awdan, Sally A., and Gihan F. Asaad. "Liver Fibrosis: Underlying Mechanisms and Innovative Therapeutic Approach. A Review Article." Biomedical and Pharmacology Journal 14, no. 4 (2021): 1841–62. http://dx.doi.org/10.13005/bpj/2283.

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Liver fibrosis is considered: “a pathological repairing process in liver injuries leading to extracellular cell matrix (ECM) accumulation evidencing chronic liver diseases”. Chronic viral hepatitis, alcohol consumption, autoimmune diseases as well as non-alcoholic steatohepatitis are from the main causes of liver fibrosis (Lee et al., 2015; Mieli-Vergani et al., 2018). Hepatic stellate cells (HSCs) exist in the sinus space next to the hepatic epithelial cells as well as endothelial cells (Yin et al., 2013). Normally, HSCs are quiescent and mainly participate in fat storage and in the metabolis

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Allen, Joselyn Natasha, Mary Kennett, Andrew Patterson, and Pamela A. Hankey-Giblin. "Loss of MSP-dependent Ron receptor signaling exacerbates liver fibrosis in a high fat high cholesterol diet-induced ApoE KO mouse model." Journal of Immunology 200, no. 1_Supplement (2018): 42.26. http://dx.doi.org/10.4049/jimmunol.200.supp.42.26.

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Abstract Liver fibrosis marks the turning point of non-alcoholic steatohepatitis and with no specific and effective anti-fibrotic therapies available, this disease is a major global health burden. Here, we established the novel role of the Ron receptor in mitigating liver fibrosis. For 18 weeks, apolipoprotein E (ApoE KO) and ApoE x Ron double knockout (DKO) mice were fed a fat and cholesterol-rich diet. Livers from DKO animals exhibited increased accumulation of sirius red-stained collagen. Immunohistochemistry of αSMA revealed that DKO livers had increased activation of collagen-producing he

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Lee, Young-Sil, Geum seo Kim, Hyo-Jeong Yun, et al. "Sa1533 LT-006, A LIVE BIOTHERAPEUTIC PRODUCT, IMPROVES HEPATIC STEATOSIS INFLAMMATION, AND FIBOROSIS IN NON-ALCHOLIC STEATOHEPATITIS (NASH) AND BILE DICT LIGATION (BDL)-INDUCED LIVER FIBROSIS ANIMAL MODELS." Gastroenterology 166, no. 5 (2024): S—1571—S—1572. http://dx.doi.org/10.1016/s0016-5085(24)04071-x.

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van den Hoek, Anita M., Serdar Özsezen, Martien P. M. Caspers, Arianne van Koppen, Roeland Hanemaaijer, and Lars Verschuren. "Unraveling the Transcriptional Dynamics of NASH Pathogenesis Affecting Atherosclerosis." International Journal of Molecular Sciences 23, no. 15 (2022): 8229. http://dx.doi.org/10.3390/ijms23158229.

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The prevalence of non-alcoholic steatohepatitis (NASH) is rapidly increasing and associated with cardiovascular disease (CVD), the major cause of mortality in NASH patients. Although sharing common risk factors, the mechanisms by which NASH may directly contribute to the development to CVD remain poorly understood. The aim of this study is to gain insight into key molecular processes of NASH that drive atherosclerosis development. Thereto, a time-course study was performed in Ldlr−/−.Leiden mice fed a high-fat diet to induce NASH and atherosclerosis. The effects on NASH and atherosclerosis wer

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Karin, Michael, Li Gu, and Yahui Zhu. "Abstract IA04: Metabolic control of HCC initiation and progression." Clinical Cancer Research 28, no. 17_Supplement (2022): IA04. http://dx.doi.org/10.1158/1557-3265.liverca22-ia04.

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Abstract Non-alcoholic steatohepatitis (NASH) is quickly becoming the leading HCC etiology. NASH can lead to HCC by altering liver metabolism, inducing oncogenic mutations, causing tumor promoting inflammation as well as the immunosuppression of anti-HCC immunity. We have established an accurate model for studying NASH-induced HCC development, the MUP-uPA mouse, and used it to show that elevated TNF production by liver macrophages contributes to both NASH and HCC progression. The major cause of TNF induction during NASH is gut-derived endotoxin, whose infiltration into the portal circulation i

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Mehal, Wajahat. "Mechanisms of liver fibrosis in metabolic syndrome." eGastroenterology 1, no. 1 (2023): e100015. http://dx.doi.org/10.1136/egastro-2023-100015.

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The understanding of the mechanisms of liver fibrosis has been dominated by models in which chronic hepatocellular injury is the initiating step as is seen with viral infections. The increased prevalence of the metabolic syndrome, and the increases in liver fibrosis due to metabolic syndrome driven non-alcoholic steatohepatitis (NASH), has made it a priority to understand how this type of liver fibrosis is similar to, and different from, pure hepatocellular injury driven liver fibrosis. Both types of liver fibrosis have the transformation of the hepatic stellate cell (HSC) into a myofibroblast

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Mohamed Ismail, Salah Tharwat, Engy Yousry El Sayed Ashour, Hesham Hamdy AL-kilani, and Khalid Abd EL-hamid Rafaat. "Serum Anandamide for Assessment of Non Alcholic Fatty Liver Disease Severity." QJM: An International Journal of Medicine 117, Supplement_2 (2024). http://dx.doi.org/10.1093/qjmed/hcae175.469.

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Abstract Background Nonalcoholic fatty liver disease (NAFLD) is a very common disease, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and is considered the hepatic expression of metabolic syndrome. Liver biopsy is currently considered the gold standard in diagnosis of NAFLD; however, it is an invasive technique and carries many risks. The serum anandamide level is recently discovered to play an important role as the potential indicator for NAFLD severity. The purpose of the study is to determine the association of endocannabinoid metabolite anandamide and NAFLD severity a

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Ipsen, D. H., R. H. Agerskov, J. H. Klaebel, J. Lykkesfeldt, and Pernille Tveden-Nyborg. "The development of nonalcoholic steatohepatitis is subjected to breeder dependent variation in guinea pigs." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-82643-0.

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AbstractVariability in disease development due to differences in strains and breeders constitutes a substantial challenge in preclinical research. However, the impact of the breeder on non-alcoholic steatohepatitis (NASH) is not yet fully elucidated. This retrospective study investigates NASH development in guinea pigs from Charles River or Envigo fed a high fat diet (20% fat, 15% sucrose, 0.35% cholesterol) for 16 or 24/25 weeks. Charles River animals displayed more severe NASH, with higher steatosis (p < 0.05 at week 16), inflammation (p < 0.05 at both week), fibrosis (p < 0.05 at w

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Thèses sur le sujet "Non Alcholic Steatohepatitis PDGF"

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LOCATELLI, LUIGI. "Expression of aVB6 integrin by Pkhd1-defective cholangiocytes links enhanced ductal secretion of Macrophage chemokines to progressive portal fibrosis in Congenital Hepatic Fibrosis." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/41733.

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BACKGROUND AND AIMS: Congenital Hepatic Fibrosis (CHF) is caused by mutations in PKHD1, a gene encoding for fibrocystin, a protein of unknown function, expressed in cholangiocyte cilia and centromers. In CHF, biliary dysgenesis is accompanied by severe progressive portal fibrosis and portal hypertension. The mechanisms responsible for portal fibrosis in CHF are unclear. The αvβ6 integrin mediates local activation of TGFβ1 and is expressed by reactive cholangiocytes during cholestasis. To understand the mechanisms of fibrosis in CHF we studied the expression of αvβ6 integrin and its regulation

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