PMID- 22459281
OWN - NLM
STAT- MEDLINE
DCOM- 20121030
LR  - 20211203
IS  - 1532-1991 (Electronic)
IS  - 0143-4160 (Print)
IS  - 0143-4160 (Linking)
VI  - 52
IP  - 1
DP  - 2012 Jul
TI  - Mitochondrial Ca(2+) signals in autophagy.
PG  - 44-51
LID - 10.1016/j.ceca.2012.03.001 [doi]
AB  - Macroautophagy (autophagy) is a lysosomal degradation pathway that is conserved 
      from yeast to humans that plays an important role in recycling cellular 
      constituents in all cells. A number of protein complexes and signaling pathways 
      impinge on the regulation of autophagy, with the mammalian target of rapamycin 
      (mTOR) as the central player in the canonical pathway. Cytoplasmic Ca(2+) 
      signaling also regulates autophagy, with both activating and inhibitory effects, 
      mediated by the canonical as well as non-canonical pathways. Here we review this 
      regulation, with a focus on the role of an mTOR-independent pathway that involves 
      the inositol trisphosphate receptor (InsP(3)R) Ca(2+) release channel and Ca(2+) 
      signaling to mitochondria. Constitutive InsP(3)R Ca(2+) transfer to mitochondria 
      is required for autophagy suppression in cells in nutrient-replete media. In its 
      absence, cells become metabolically compromised due to insufficient production of 
      reducing equivalents to support oxidative phosphorylation. Absence of this Ca(2+) 
      transfer to mitochondria results in activation of AMPK, which activates 
      mTOR-independent pro-survival autophagy. Constitutive InsP(3)R Ca(2+) release to 
      mitochondria is an essential cellular process that is required for efficient 
      mitochondrial respiration, maintenance of normal cell bioenergetics and 
      suppression of autophagy.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Cardenas, Cesar
AU  - Cardenas C
AD  - Department of Physiology, University of Pennsylvania, Philadelphia, PA 
      19104-6085, USA.
FAU - Foskett, J Kevin
AU  - Foskett JK
LA  - eng
GR  - GM/DK56328/DK/NIDDK NIH HHS/United States
GR  - R37 GM056328/GM/NIGMS NIH HHS/United States
GR  - R01 MH059937-14/MH/NIMH NIH HHS/United States
GR  - R37 GM056328-14/GM/NIGMS NIH HHS/United States
GR  - R01 MH059937/MH/NIMH NIH HHS/United States
GR  - R01 DK056328/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20120328
PL  - Netherlands
TA  - Cell Calcium
JT  - Cell calcium
JID - 8006226
RN  - 0 (Inositol 1,4,5-Trisphosphate Receptors)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.3 (AMP-Activated Protein Kinase Kinases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - AMP-Activated Protein Kinase Kinases
MH  - *Autophagy
MH  - Calcium/metabolism
MH  - *Calcium Signaling
MH  - Humans
MH  - Inositol 1,4,5-Trisphosphate Receptors/metabolism
MH  - Mitochondria/*metabolism
MH  - Protein Kinases/metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
PMC - PMC3389293
MID - NIHMS363011
EDAT- 2012/03/31 06:00
MHDA- 2012/10/31 06:00
PMCR- 2013/07/01
CRDT- 2012/03/31 06:00
PHST- 2012/01/17 00:00 [received]
PHST- 2012/02/29 00:00 [revised]
PHST- 2012/03/01 00:00 [accepted]
PHST- 2012/03/31 06:00 [entrez]
PHST- 2012/03/31 06:00 [pubmed]
PHST- 2012/10/31 06:00 [medline]
PHST- 2013/07/01 00:00 [pmc-release]
AID - S0143-4160(12)00052-8 [pii]
AID - 10.1016/j.ceca.2012.03.001 [doi]
PST - ppublish
SO  - Cell Calcium. 2012 Jul;52(1):44-51. doi: 10.1016/j.ceca.2012.03.001. Epub 2012 
      Mar 28.