PMID- 30307158
OWN - NLM
STAT- MEDLINE
DCOM- 20191028
LR  - 20210902
IS  - 1479-6813 (Electronic)
IS  - 0952-5041 (Print)
IS  - 0952-5041 (Linking)
VI  - 61
IP  - 3
DP  - 2018 Oct 1
TI  - The mitochondrial unfolded protein response and mitohormesis: a perspective on 
      metabolic diseases.
PG  - R91-R105
LID - 10.1530/JME-18-0005 [doi]
AB  - Mitochondria perform essential roles as crucial organelles for cellular and 
      systemic energy homeostasis, and as signaling hubs, which coordinate nuclear 
      transcriptional responses to the intra- and extra-cellular environment. Complex 
      human diseases, including diabetes, obesity, fatty liver disease and 
      aging-related degenerative diseases are associated with alterations in 
      mitochondrial oxidative phosphorylation (OxPhos) function. However, a recent 
      series of studies in animal models have revealed that an integrated response to 
      tolerable mitochondrial stress appears to render cells less susceptible to 
      subsequent aging processes and metabolic stresses, which is a key feature of 
      mitohormesis. The mitochondrial unfolded protein response (UPRmt) is a central 
      part of the mitohormetic response and is a retrograde signaling pathway, which 
      utilizes the mitochondria-to-nucleus communication network. Our understanding of 
      the UPRmt has contributed to elucidating the role of mitochondria in metabolic 
      adaptation and lifespan regulation. In this review, we discuss and integrate 
      recent data from the literature on the present status of mitochondrial OxPhos 
      function in the development of metabolic diseases, relying on evidence from human 
      and other animal studies, which points to alterations in mitochondrial function 
      as a key factor in the regulation of metabolic diseases and conclude with a 
      discussion on the specific roles of UPRmt and mitohormesis as a novel therapeutic 
      strategy for the treatment of obesity and insulin resistance.
CI  - (c) 2018 The authors 2018
FAU - Yi, Hyon-Seung
AU  - Yi HS
AD  - Research Center for Endocrine and Metabolic Diseases, Chungnam National 
      University School of Medicine, Daejeon, Korea
FAU - Chang, Joon Young
AU  - Chang JY
AD  - Research Center for Endocrine and Metabolic Diseases, Chungnam National 
      University School of Medicine, Daejeon, Korea
AD  - Department of Medical Science, Chungnam National University School of Medicine, 
      Daejeon, Korea
FAU - Shong, Minho
AU  - Shong M
AD  - Research Center for Endocrine and Metabolic Diseases, Chungnam National 
      University School of Medicine, Daejeon, Korea
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20181001
PL  - England
TA  - J Mol Endocrinol
JT  - Journal of molecular endocrinology
JID - 8902617
SB  - IM
MH  - Animals
MH  - Humans
MH  - Insulin Resistance/physiology
MH  - Metabolic Diseases/metabolism
MH  - Mitochondria/*metabolism
MH  - Oxidative Phosphorylation
MH  - Signal Transduction/physiology
MH  - Unfolded Protein Response/physiology
PMC - PMC6145237
OTO - NOTNLM
OT  - mitochondria
OT  - oxidative phosphorylation
OT  - mitochondrial unfolded protein response
OT  - diabetes
OT  - insulin resistance
COIS- The authors declare that there is no conflict of interest that could be perceived 
      as prejudicing the impartiality of this review.
EDAT- 2018/10/12 06:00
MHDA- 2019/10/29 06:00
PMCR- 2018/09/19
CRDT- 2018/10/12 06:00
PHST- 2018/10/12 06:00 [entrez]
PHST- 2018/10/12 06:00 [pubmed]
PHST- 2019/10/29 06:00 [medline]
PHST- 2018/09/19 00:00 [pmc-release]
AID - JME180005 [pii]
AID - 10.1530/JME-18-0005 [doi]
PST - epublish
SO  - J Mol Endocrinol. 2018 Oct 1;61(3):R91-R105. doi: 10.1530/JME-18-0005.