Journal
AUTOPHAGY
Volume 11, Issue 7, Pages 1207-1208Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2015.1052209
Keywords
atherosclerosis; autophagy; ER stress; free cholesterol; LC3; ORMDL1; p62; serine palmitoyl-CoA transferase; sphingomyelin
Categories
Funding
- NHLBI NIH HHS [P01 HL029582, P01 HL098055] Funding Source: Medline
Ask authors/readers for more resources
Cholesterol confers unique biophysical properties to the plasma membrane bilayer that are essential for maintaining optimal membrane fluidity, which in turn regulate multiple physiological functions required to promote cellular integrity and viability. Conversely, excessive cholesterol causes pathological conditions such as atherosclerosis that can lead to heart attacks. Human atheroma macrophages carry a large burden of free cholesterol (FC) in addition to cholesterol esters. It is recognized that sterols can modulate the levels of other lipids to attain lipid homeostasis; thus, excess FC may play a role in modulating compensatory sphingolipid pathways. Recent studies have shown that excess lipids can cause ER stress and apoptosis. In contrast, autophagy may play a protective role by clearing excess lipids from macrophage foam cell lipid droplets. Interestingly, a macrophage study using a TLR4-specifc agonist showed that de novo sphingolipid biosynthesis is essential for autophagy induction, suggesting links between sphingolipid biosynthesis and autophagy. While the role of autophagy in removing excess lipids has been the focus of many studies, its role in fine-tuning cellular lipid homeostasis remains largely unexplored.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available