Abstract
Background and Aims : The prevalence of non-alcoholic steatohepatitis (NASH) is rapidly increasing and associated with cardiovascular disease (CVD), the major cause of mortality in NASH patients. Although sharing common risk factors, the mechanisms by which NASH may directly contribute to the development to CVD remain poorly understood. The aim of this study was to gain insight into the dynamics of key molecular processes of NASH that drive atherosclerosis development.
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