Perspectives on Mitochondria–ER and Mitochondria–Lipid Droplet Contact in Hepatocytes and Hepatic Lipid Metabolism

Emerging evidence suggests that mitochondrion–endoplasmic reticulum (ER) and mitochondrion–lipid droplet (LD) contact sites are critical in regulating lipid metabolism in cells. It is well established that intracellular organelles communicate with each other continuously through membrane contact sit...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2021-09, Vol.10 (9), p.2273
Main Authors: Ma, Xiaowen, Qian, Hui, Chen, Allen, Ni, Hong-Min, Ding, Wen-Xing
Format: Article
Language:English
Subjects:
alcohol
Apoptosis
autophagy
Biosynthesis
Endoplasmic reticulum
Enzymes
Fatty acids
Fatty liver
Hepatocytes
Homeostasis
Lipid metabolism
Lipids
lipophagy
lipotoxicity
Liver diseases
Mammals
Membranes
Metabolism
Metabolites
Microscopy
Mitochondria
NAFLD
Organelles
Physiology
Proteins
Review
Roles
Signal transduction
starvation
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Summary:Emerging evidence suggests that mitochondrion–endoplasmic reticulum (ER) and mitochondrion–lipid droplet (LD) contact sites are critical in regulating lipid metabolism in cells. It is well established that intracellular organelles communicate with each other continuously through membrane contact sites to maintain organelle function and cellular homeostasis. The accumulation of LDs in hepatocytes is an early indicator of non-alcoholic fatty liver disease (NAFLD) and alcohol-related liver disease (ALD), which may indicate a breakdown in proper inter-organelle communication. In this review, we discuss previous findings in mitochondrion–ER and mitochondrion–LD contact, focusing on their roles in lipid metabolism in hepatocytes. We also present evidence of a unique mitochondrion–LD contact structure in hepatocytes under various physiological and pathological conditions and propose a working hypothesis to speculate about the role of these structures in regulating the functions of mitochondria and LDs and their implications in NAFLD and ALD.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells10092273