PMID- 32998777
OWN - NLM
STAT- MEDLINE
DCOM- 20210802
LR  - 20240331
IS  - 1476-511X (Electronic)
IS  - 1476-511X (Linking)
VI  - 19
IP  - 1
DP  - 2020 Sep 30
TI  - Signaling and other functions of lipids in autophagy: a review.
PG  - 214
LID - 10.1186/s12944-020-01389-2 [doi]
LID - 214
AB  - The process of autophagy is integral to cellular function. In this process, 
      proteins, organelles, and metabolites are engulfed in a lipid vesicle and 
      trafficked to a lysosome for degradation. Its central role in protein and 
      organelle homeostasis has piqued interest for autophagy dysfunction as a driver 
      of pathology for a number of diseases including cancer, muscular disorders, 
      neurological disorders, and non-alcoholic fatty liver disease. For much of its 
      history, the study of autophagy has centered around proteins, however, due to 
      advances in mass spectrometry and refined methodologies, the role of lipids in 
      this essential cellular process has become more apparent. This review discusses 
      the diverse endogenous lipid compounds shown to mediate autophagy. Downstream 
      lipid signaling pathways are also reviewed in the context of autophagy 
      regulation. Specific focus is placed upon the Mammalian Target of Rapamycin 
      (mTOR) and Peroxisome Proliferator-Activated Receptor (PPAR) signaling pathways 
      as integration hubs for lipid regulation of autophagy.
FAU - Soto-Avellaneda, Alejandro
AU  - Soto-Avellaneda A
AUID- ORCID: 0000-0003-2600-9639
AD  - Biomolecular Sciences Graduate programs, Boise State University, Boise, ID, 
      83725, USA.
FAU - Morrison, Brad E
AU  - Morrison BE
AD  - Biomolecular Sciences Graduate programs, Boise State University, Boise, ID, 
      83725, USA. bradmorrison@boisestate.edu.
AD  - Department of Biological Sciences, Boise State University, Boise, ID, 83725, USA. 
      bradmorrison@boisestate.edu.
LA  - eng
GR  - P20GM103408/GM/NIGMS NIH HHS/United States
GR  - R15NS096702/NS/NINDS NIH HHS/United States
GR  - P20 GM103408/GM/NIGMS NIH HHS/United States
GR  - R15 NS096702/NS/NINDS NIH HHS/United States
GR  - P20 GM109095/GM/NIGMS NIH HHS/United States
GR  - P20GM109095/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20200930
PL  - England
TA  - Lipids Health Dis
JT  - Lipids in health and disease
JID - 101147696
RN  - 0 (Lipids)
RN  - 0 (Peroxisome Proliferator-Activated Receptors)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Autophagy/*genetics
MH  - Homeostasis/genetics
MH  - Humans
MH  - Lipids/*genetics
MH  - Lysosomes/genetics
MH  - Peroxisome Proliferator-Activated Receptors/*genetics
MH  - Protein Transport/genetics
MH  - Signal Transduction/genetics
MH  - TOR Serine-Threonine Kinases/*genetics
PMC - PMC7525950
OTO - NOTNLM
OT  - Autophagy
OT  - Fatty acids
OT  - Lipids
OT  - Mammalian target of rapamycin
OT  - Peroxisome proliferator-activated receptor
OT  - Phospholipids
OT  - Sphingolipids
COIS- The authors declare they have no competing interests.
EDAT- 2020/10/02 06:00
MHDA- 2021/08/03 06:00
PMCR- 2020/09/30
CRDT- 2020/10/01 05:27
PHST- 2020/08/07 00:00 [received]
PHST- 2020/09/23 00:00 [accepted]
PHST- 2020/10/01 05:27 [entrez]
PHST- 2020/10/02 06:00 [pubmed]
PHST- 2021/08/03 06:00 [medline]
PHST- 2020/09/30 00:00 [pmc-release]
AID - 10.1186/s12944-020-01389-2 [pii]
AID - 1389 [pii]
AID - 10.1186/s12944-020-01389-2 [doi]
PST - epublish
SO  - Lipids Health Dis. 2020 Sep 30;19(1):214. doi: 10.1186/s12944-020-01389-2.