Abstract
Non-alcoholic fatty liver disease (NAFLD), an accumulation of intra-hepatic triglycerides that is often considered the hepatic manifestation of insulin resistance, is the most common cause of chronic liver disease in the Western countries with up to one third of the population affected. NAFLD is a spectrum of disturbances that encompasses various degrees of liver damage ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). NASH is characterized by hepatocellular injury/inflammation with or without fibrosis. The individuals with NAFLD develop NASH in 10% of the cases, and are also at risk of developing hepatocellular carcinoma (HCC). Epigenetic mechanisms of nuclear chromatin remodeling, such as DNA methylation, post-translational modifications of histones, and incorporation of histone variants into the chromatin are increasingly recognized as crucial factors in the pathophysiology of NAFLD. NAFLD is often accompanied by oxidative stress: reactive oxygen species (ROS) are implicated in altered reduction/oxidation (redox) reactions that attack cellular macromolecules and are detected in the liver of patients and animal models of NAFLD. In this review, we summarize recent knowledge advancements in the hepatic epigenetic and redox mechanisms, and their possible links, involved in the pathogenesis and treatment of NAFLD.
| Original language | English |
|---|---|
| Pages (from-to) | 2737-2746 |
| Number of pages | 10 |
| Journal | Current Pharmaceutical Design |
| Volume | 19 |
| Issue number | 15 |
| DOIs | |
| Publication status | Published - 2013 |
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Keywords
- Epigenetics
- Non-alcoholic fatty liver disease (NAFLD)
- Oxidative stress
ASJC Scopus subject areas
- Drug Discovery
- Pharmacology
Cite this
Redox homeostasis and epigenetics in non-alcoholic fatty liver disease (NAFLD). / Podrini, Christine; Borghesan, Michela; Greco, Azzura; Pazienza, Valerio; Mazzoccoli, Gianluigi; Vinciguerra, Manlio.
In: Current Pharmaceutical Design, Vol. 19, No. 15, 2013, p. 2737-2746.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Redox homeostasis and epigenetics in non-alcoholic fatty liver disease (NAFLD)
AU - Podrini, Christine
AU - Borghesan, Michela
AU - Greco, Azzura
AU - Pazienza, Valerio
AU - Mazzoccoli, Gianluigi
AU - Vinciguerra, Manlio
PY - 2013
Y1 - 2013
N2 - Non-alcoholic fatty liver disease (NAFLD), an accumulation of intra-hepatic triglycerides that is often considered the hepatic manifestation of insulin resistance, is the most common cause of chronic liver disease in the Western countries with up to one third of the population affected. NAFLD is a spectrum of disturbances that encompasses various degrees of liver damage ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). NASH is characterized by hepatocellular injury/inflammation with or without fibrosis. The individuals with NAFLD develop NASH in 10% of the cases, and are also at risk of developing hepatocellular carcinoma (HCC). Epigenetic mechanisms of nuclear chromatin remodeling, such as DNA methylation, post-translational modifications of histones, and incorporation of histone variants into the chromatin are increasingly recognized as crucial factors in the pathophysiology of NAFLD. NAFLD is often accompanied by oxidative stress: reactive oxygen species (ROS) are implicated in altered reduction/oxidation (redox) reactions that attack cellular macromolecules and are detected in the liver of patients and animal models of NAFLD. In this review, we summarize recent knowledge advancements in the hepatic epigenetic and redox mechanisms, and their possible links, involved in the pathogenesis and treatment of NAFLD.
AB - Non-alcoholic fatty liver disease (NAFLD), an accumulation of intra-hepatic triglycerides that is often considered the hepatic manifestation of insulin resistance, is the most common cause of chronic liver disease in the Western countries with up to one third of the population affected. NAFLD is a spectrum of disturbances that encompasses various degrees of liver damage ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). NASH is characterized by hepatocellular injury/inflammation with or without fibrosis. The individuals with NAFLD develop NASH in 10% of the cases, and are also at risk of developing hepatocellular carcinoma (HCC). Epigenetic mechanisms of nuclear chromatin remodeling, such as DNA methylation, post-translational modifications of histones, and incorporation of histone variants into the chromatin are increasingly recognized as crucial factors in the pathophysiology of NAFLD. NAFLD is often accompanied by oxidative stress: reactive oxygen species (ROS) are implicated in altered reduction/oxidation (redox) reactions that attack cellular macromolecules and are detected in the liver of patients and animal models of NAFLD. In this review, we summarize recent knowledge advancements in the hepatic epigenetic and redox mechanisms, and their possible links, involved in the pathogenesis and treatment of NAFLD.
KW - Epigenetics
KW - Non-alcoholic fatty liver disease (NAFLD)
KW - Oxidative stress
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UR - http://www.scopus.com/inward/citedby.url?scp=84876727580&partnerID=8YFLogxK
U2 - 10.2174/1381612811319150009
DO - 10.2174/1381612811319150009
M3 - Article
C2 - 23092327
AN - SCOPUS:84876727580
VL - 19
SP - 2737
EP - 2746
JO - Current Pharmaceutical Design
JF - Current Pharmaceutical Design
SN - 1381-6128
IS - 15
ER -