Current NASH Pathogenesis and Diagnostic Techniques and Treatments
DOI:
https://doi.org/10.54097/hset.v36i.6281Keywords:
Non-alcoholic steatohepatitis, Pathogenesis, Protein inhibition, Models.Abstract
Nonalcoholic fatty liver disease (NAFLD) is defined by excessive triglyceride deposition in liver, excluding alcoholic or drug factors. NAFLD has grown into a public health concern since it is a leading cause of chronic liver disease in wealthy areas due to obesity and its associated metabolic syndrome. NAFLD has two typical types: non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH). NASH significantly impacts the life quality and life expectancy of chronic liver disease. Moreover, NASH is fatal since it involves the onset of multiple chronic disease and may cause cirrhosis and liver failure. Potentially more worrying, NASH does not show any obvious symptoms in early stages, therefore, a more effective and precise NASH diagnostic technique is necessary. This review introduces the current research status of NASH and summarizes the obstacles and potential solution in this research.
Downloads
References
Friedman, S.L.; et al. Mechanisms of NAFLD Development and Therapeutic Strategies. Nature Medicine. 2018: 1.
Alkhouri, N.; et al. Apoptosis in Nonalcoholic Fatty Liver Disease: Diagnostic and Therapeutic Implications. Expert Review of Gastroenterology & Hepatology. 2011, 5 (2): 201 - 212.
Alisi, A.; et al. Intrauterine Growth Retardation and Nonalcoholic Fatty Liver Disease in Children. International Journal of Endocrinology. 2011.
Eguchi, A.; et al. Biomarkers of Liver Cell Death. Journal of Hepatology. 2014, 60 (5): 1063 - 1074.
Ruttkay-Nedecky, B.; et al. The Role of Metallothionein in Oxidative Stress. International Journal of Molecular Sciences. 2013, 14 (3): 6044 - 6066.
Musso, G.; et al. Non-alcoholic Steatohepatitis: Emerging Molecular Targets and Therapeutic Strategies. Nature Reviews Drug Discovery. 2016, 15 (4): 249 - 74.
Peverill, W.; et al. Evolving Concepts in the Pathogenesis of NASH: Beyond Steatosis and Inflammation. International Journal of Molecular Sciences. 2014, 15 (5): 8591 - 8638.
Mridha, A.R.; et al. NLRP3 Inflammasome Blockade Reduces Liver Inflammation and Fibrosis in Experimental NASH in Mice. Journal Of Hepatology. 2017, 66 (5): 1037 - 1046.
Mazza, G.; et al. Engineering in Vitro Models of Hepatofibrogenesis. Advanced Drug Delivery Reviews. 2017, 121: 147 - 157.
Ibrahim, S.H.; et al. Non-Alcoholic Steatohepatitis Pathogenesis: Sublethal Hepatocyte Injury as A Driver of Liver Inflammation.
Shimano, H.; Sato, R. SREBP-Regulated Lipid Metabolism: Convergent Physiology-Divergent Pathophysiology. Nature Reviews Endocrinology. 2017.
Shapiro, H.; et al. Bile Acids in Glucose Metabolism in Health and Disease. Journal of Experimental Medicine. 2018, 215 (2): 383 - 396.
Zammit, V. A. Hepatic Triacylglycerol Synthesis and Secretion: DGAT2 as the Link Between Glycaemia and Triglyceridaemia. Biochemical Journal. 2013, 451 (1).
Win, S.; et al. New Insights into the Role and Mechanism of C-Jun-N-Terminal Kinase Signaling in the Pathobiology of Liver Diseases. Hepatology. 2018, 67 (5): 2013 - 2024.
Kodama, Y.; Brenner, D.A. c-Jun N-terminal kinase signaling in the pathogenesis of nonalcoholic fatty liver disease: Multiple roles in multiple steps. Hepatology. 2009, 49 (1): 6 - 8.
Schuster, S.; Feldstein, A.E. Nash: Novel Therapeutic Strategies Targeting Ask1 in NASH. Nature Reviews Gastroenterology & Hepatology. 2017.
Downloads
Published
Issue
Section
License

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.







