PMID- 30974387
OWN - NLM
STAT- MEDLINE
DCOM- 20190829
LR  - 20190829
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 114
DP  - 2019 Jun
TI  - ACE inhibitor suppresses cardiac remodeling after myocardial infarction by 
      regulating dendritic cells and AT(2) receptor-mediated mechanism in mice.
PG  - 108660
LID - S0753-3322(18)38058-2 [pii]
LID - 10.1016/j.biopha.2019.108660 [doi]
AB  - Dendritic cells (DCs) play a complex role in the progression of myocardial 
      infarction (MI). The impact of angiotensin-converting enzyme (ACE) inhibitor 
      therapy, partly via affecting DCs maturation and recruitment, was tested on a MI 
      mouse model. Furthermore, the cardioprotective effects of ACEI were enhanced 
      through attenuating migration of DCs from the spleen into peripheral circulation, 
      thereby inhibiting DCs maturation and tissue inflammation. ACEI repress DCs 
      immune inflammatory response through down-regulating DCs maturation surface 
      markers and regulating inflammatory cytokines, which led to a higher survival 
      rate, improved function and remodeling through decreased inflammatory response 
      after MI. However, inhibition of AT(2)R activation, resulted in a reduction of 
      ACEI effects on DCs. The potent anti-inflammatory effect of ACEI can partially be 
      attributed to its impact on DCs through activation of AT(2)R, which may provide a 
      new target mechanism for ACEI therapy after MI.
CI  - Copyright (c) 2019 The Authors. Published by Elsevier Masson SAS.. All rights 
      reserved.
FAU - Ma, Yuanji
AU  - Ma Y
AD  - Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China; 
      Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
FAU - Yuan, Jie
AU  - Yuan J
AD  - Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
FAU - Hu, Jialu
AU  - Hu J
AD  - Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China; 
      Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
FAU - Gao, Wei
AU  - Gao W
AD  - Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China; 
      Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
FAU - Zou, Yunzeng
AU  - Zou Y
AD  - Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China; 
      Shanghai Institute of Cardiovascular Diseases, Shanghai, China.
FAU - Ge, Junbo
AU  - Ge J
AD  - Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China; 
      Shanghai Institute of Cardiovascular Diseases, Shanghai, China. Electronic 
      address: jbge@zs-hospital.sh.cn.
LA  - eng
PT  - Journal Article
DEP - 20190408
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Receptor, Angiotensin, Type 2)
SB  - IM
MH  - Angiotensin Receptor Antagonists/pharmacology
MH  - Angiotensin-Converting Enzyme Inhibitors/*pharmacology
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Dendritic Cells/*drug effects
MH  - Disease Models, Animal
MH  - Down-Regulation/drug effects
MH  - Heart/*drug effects
MH  - Inflammation/drug therapy/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myocardial Infarction/*drug therapy/metabolism
MH  - Myocardium/metabolism
MH  - Receptor, Angiotensin, Type 2/*metabolism
MH  - Survival Rate
MH  - Ventricular Remodeling/*drug effects
OTO - NOTNLM
OT  - ACE inhibitor
OT  - AT(2) receptor
OT  - Dendritic cell
OT  - Inflammation
OT  - Myocardial infarction
EDAT- 2019/04/12 06:00
MHDA- 2019/08/30 06:00
CRDT- 2019/04/12 06:00
PHST- 2018/11/13 00:00 [received]
PHST- 2019/01/31 00:00 [revised]
PHST- 2019/02/01 00:00 [accepted]
PHST- 2019/04/12 06:00 [pubmed]
PHST- 2019/08/30 06:00 [medline]
PHST- 2019/04/12 06:00 [entrez]
AID - S0753-3322(18)38058-2 [pii]
AID - 10.1016/j.biopha.2019.108660 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2019 Jun;114:108660. doi: 10.1016/j.biopha.2019.108660. Epub 
      2019 Apr 8.