PMID- 30367996
OWN - NLM
STAT- MEDLINE
DCOM- 20200217
LR  - 20200217
IS  - 1873-4596 (Electronic)
IS  - 0891-5849 (Linking)
VI  - 130
DP  - 2019 Jan
TI  - Soluble receptor for advance glycation end-products inhibits 
      ischemia/reperfusion-induced myocardial autophagy via the STAT3 pathway.
PG  - 107-119
LID - S0891-5849(18)31365-0 [pii]
LID - 10.1016/j.freeradbiomed.2018.10.437 [doi]
AB  - The pathogenesis of myocardial ischemia/reperfusion (I/R) is poorly understood, 
      but recent evidence suggests that autophagy plays crucial roles in I/R injuries. 
      Soluble receptor for advanced glycation end-products (sRAGE) exerts protective 
      effects during I/R by decreasing cardiac apoptosis, which is mediated via 
      increasing the ubiquitin proteasome system (UPS) and signal transducer and 
      activator of transcription 3 (STAT3). The present study examined the effects and 
      mechanisms of sRAGE on I/R-triggered cardiac autophagy. I/R was performed in mice 
      or primary neonatal cardiomyocytes with or without sRAGE administration or 
      overexpression. Cardiac function and infarct size were detected in mouse hearts. 
      Apoptosis, autophagy and autophagy-related signaling pathways were detected in 
      mouse hearts and cardiomyocytes. The results demonstrated that sRAGE 
      significantly improved cardiac function and reduced infarct size during I/R in 
      mice. sRAGE inhibited I/R-induced apoptosis, which correlated with a reduction in 
      autophagy-associated proteins, including ATG7, Beclin-1 and 
      microtubule-associated protein 1 light chain 3 (LC3). sRAGE reduced autophagosome 
      formation during I/R in vivo and in vitro. sRAGE significantly activated STAT3, 
      but not mammalian target of rapamycin (mTOR), during I/R in vivo and in vitro, 
      and suppression of STAT3 abolished the sRAGE inhibition of autophagy during I/R 
      in vitro. Activation of autophagy using ATG7 overexpression with an adenovirus 
      significantly abolished the sRAGE-induced reduction of cardiac apoptosis during 
      I/R. These results suggest that sRAGE inhibits I/R injuries in the heart via a 
      decrease in autophagy, a process that is dependent on STAT3 activation.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Dang, Mengqiu
AU  - Dang M
AD  - Department of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, 
      6 Tiantan Xili, Dongcheng District, Beijing 100050, China.
FAU - Zeng, Xiangjun
AU  - Zeng X
AD  - Department of Physiology and Pathophysiology, Capital Medical University, Beijing 
      100069, China.
FAU - Chen, Buxing
AU  - Chen B
AD  - Department of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, 
      6 Tiantan Xili, Dongcheng District, Beijing 100050, China.
FAU - Wang, Hongxia
AU  - Wang H
AD  - Department of Physiology and Pathophysiology, Capital Medical University, Beijing 
      100069, China.
FAU - Li, Huihua
AU  - Li H
AD  - Department of Cardiology, Institute of cardiovascular Disease, First Affiliated 
      Hospital of Dalian Medical University, Dalian 116011, China; Department of 
      Nutrition and Food Hygiene, School of Public Health, Advanced Institute of 
      Medical Sciences, Dalian Medical University, Dalian 116044, China.
FAU - Liu, Yu
AU  - Liu Y
AD  - Department of Physiology and Pathophysiology, Capital Medical University, Beijing 
      100069, China.
FAU - Zhang, Xiuling
AU  - Zhang X
AD  - Department of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, 
      6 Tiantan Xili, Dongcheng District, Beijing 100050, China.
FAU - Cao, Xianxian
AU  - Cao X
AD  - Department of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, 
      6 Tiantan Xili, Dongcheng District, Beijing 100050, China.
FAU - Du, Fenghe
AU  - Du F
AD  - Department of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, 
      6 Tiantan Xili, Dongcheng District, Beijing 100050, China; Department of 
      Geriatrics, Beijing Tian Tan Hospital, Capital Medical University, 6 Tiantan 
      Xili, Dongcheng District, Beijing 100050, China.
FAU - Guo, Caixia
AU  - Guo C
AD  - Department of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, 
      6 Tiantan Xili, Dongcheng District, Beijing 100050, China. Electronic address: 
      cxguo@ccmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181025
PL  - United States
TA  - Free Radic Biol Med
JT  - Free radical biology & medicine
JID - 8709159
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - 0 (STAT3 Transcription Factor)
RN  - EC 6.2.1.45 (Autophagy-Related Protein 7)
SB  - IM
MH  - Animals
MH  - Autophagy
MH  - Autophagy-Related Protein 7/genetics/metabolism
MH  - Cells, Cultured
MH  - Glycation End Products, Advanced/*metabolism
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myocardium/*metabolism
MH  - Myocytes, Cardiac/*physiology
MH  - Receptor for Advanced Glycation End Products/*metabolism
MH  - Reperfusion Injury/*metabolism
MH  - STAT3 Transcription Factor/metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Autophagy
OT  - I/R
OT  - Myocardium
OT  - SRAGE
OT  - STAT3
EDAT- 2018/10/28 06:00
MHDA- 2020/02/18 06:00
CRDT- 2018/10/28 06:00
PHST- 2018/08/06 00:00 [received]
PHST- 2018/10/20 00:00 [revised]
PHST- 2018/10/22 00:00 [accepted]
PHST- 2018/10/28 06:00 [pubmed]
PHST- 2020/02/18 06:00 [medline]
PHST- 2018/10/28 06:00 [entrez]
AID - S0891-5849(18)31365-0 [pii]
AID - 10.1016/j.freeradbiomed.2018.10.437 [doi]
PST - ppublish
SO  - Free Radic Biol Med. 2019 Jan;130:107-119. doi: 
      10.1016/j.freeradbiomed.2018.10.437. Epub 2018 Oct 25.