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©2014 Baishideng Publishing Group Inc.
World J Gastroenterol. Oct 21, 2014; 20(39): 14185-14204
Published online Oct 21, 2014. doi: 10.3748/wjg.v20.i39.14185
Published online Oct 21, 2014. doi: 10.3748/wjg.v20.i39.14185
Increased fibrosis with reduced percentage of fat on liver biopsy[3,4]; decreased size mirroring decreased hepatic blood flow[5] |
Loss of regenerative capacity, i.e. “replicative senescence” involving cross talks of growth hormone, glycogen synthase kinase 3β and cyclin D3 and shortening of telomeric ends of chromosomes[5,6] |
Increased inflammatory changes, hence the definition of “inflamm-aging” which, in its turn, has a detrimental effect on the regenerative response[7] |
Defective autophagy[8,9] |
Decrease in hepatic free radical scavenging system leads to increased oxidative stress resulting mainly from non-enzymatic processes in the liver[5] and is exacerbated by ethanol drinking[10] |
- Citation: Bertolotti M, Lonardo A, Mussi C, Baldelli E, Pellegrini E, Ballestri S, Romagnoli D, Loria P. Nonalcoholic fatty liver disease and aging: Epidemiology to management. World J Gastroenterol 2014; 20(39): 14185-14204
- URL: https://www.wjgnet.com/1007-9327/full/v20/i39/14185.htm
- DOI: https://dx.doi.org/10.3748/wjg.v20.i39.14185