| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5950072 | Atherosclerosis | 2011 | 8 Pages |
Abstract
NASH, but not SS, may increase atherosclerotic and cardiovascular risk by local overexpression of mediators of atherogenesis, endothelial damage, and regulators of blood pressure; this observation may have therapeutic implications, because ACE inhibitors may improve both cardiovascular outcomes and liver fibrosis. Hepatocyte hypoxia seems to have an important role in the molecular events activated by liver steatosis.
Keywords
BIRC3MMP1IL4IL1AsICAM-1PPARGCSF2IL3SerpinB2IL6PAI-1LIFACENAFLDangiotensin I-converting enzymenonalcoholic steatohepatitisinterleukinInterleukin 1 alphaInterleukin 3Interleukin 4plasminogen activator inhibitorNonalcoholic fatty liver diseaseMetabolic syndromeleukemia inhibitory factorIntercellular adhesion molecule 1Nash C-reactive proteinCRPPeroxisome proliferator-activated receptor gamma
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Authors
Silvia Sookoian, Tomas Fernández Gianotti, Maria Soledad Rosselli, Adriana L. Burgueño, Gustavo O. Castaño, Carlos J. Pirola,