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Abstract
<p class="first" id="d6047816e69">Lipid droplets (LDs) are complex and metabolically
active organelles. They are composed
of a neutral lipid core surrounded by a monolayer of phospholipids and proteins. LD
accumulation in hepatocytes is the distinctive characteristic of non-alcoholic fatty
liver disease (NAFLD), which is a chronic, heterogeneous liver condition that can
progress to liver fibrosis and hepatocellular carcinoma. Though recent research has
improved our understanding of the mechanisms linking LD accumulation to NAFLD progression,
numerous aspects of LD biology are either poorly understood or unknown. In this review,
we provide a description of several key mechanisms that contribute to LD accumulation
in hepatocytes, favouring NAFLD progression. First, we highlight the importance of
LD architecture and describe how the dysregulation of LD biogenesis leads to endoplasmic
reticulum stress and inflammation. This is followed by an analysis of the causal nexus
that exists between LD proteome composition and LD degradation. Finally, we describe
how the increase in size of LDs causes activation of hepatic stellate cells, leading
to liver fibrosis and hepatocellular carcinoma. We conclude that acquiring a more
sophisticated understanding of LD biology will provide crucial insights into the heterogeneity
of NAFLD and assist in the development of therapeutic approaches for this liver disease.
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