Copyright
©The Author(s) 2015.
World J Gastrointest Oncol. Dec 15, 2015; 7(12): 473-483
Published online Dec 15, 2015. doi: 10.4251/wjgo.v7.i12.473
Published online Dec 15, 2015. doi: 10.4251/wjgo.v7.i12.473
Figure 2 Histone deacetylases in acute and chronic pancreatitis.
HDACs induce key pro-inflammatory mediators in AP and CP leading to destruction of pancreatic tissue with necrosis in case of AP and fibrosis/atrophy in case of CP. Inhibition of HDACs by HDACis was shown to significantly antagonist these effects in vitro and in vivo. HDAC: Histone deacetylases; HDACis: Histone deacetylases inhibitors; NG: Neutrophil granulocyte; IL: Interleukin; TNF: Tumor necrosis factor; PDGF: Platelet-derived growth factor; TGF: Transforming growth factor; SAHA: Suberoylanilide hydroxamic acid; SB: Sodium butyrate; TSA: Trichostatin A.
- Citation: Klieser E, Swierczynski S, Mayr C, Schmidt J, Neureiter D, Kiesslich T, Illig R. Role of histone deacetylases in pancreas: Implications for pathogenesis and therapy. World J Gastrointest Oncol 2015; 7(12): 473-483
- URL: https://www.wjgnet.com/1948-5204/full/v7/i12/473.htm
- DOI: https://dx.doi.org/10.4251/wjgo.v7.i12.473