Journal
CELLS
Volume 10, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/cells10092273
Keywords
alcohol; autophagy; lipophagy; lipotoxicity; NAFLD; starvation; steatosis
Categories
Funding
- National Institutes of Health [R37 AA020518, R01 DK102142, U01 AA024733, R01 AG072895, R56DK129234]
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Mitochondrion-ER and mitochondrion-LD contact sites play critical roles in regulating lipid metabolism in cells, with organelles communicating through membrane contact sites to maintain cellular homeostasis. Accumulation of lipid droplets in hepatocytes may indicate diseases such as NAFLD, highlighting the importance of proper inter-organelle communication.
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.
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