PMID- 28039466
OWN - NLM
STAT- MEDLINE
DCOM- 20180222
LR  - 20181113
IS  - 1949-2553 (Electronic)
IS  - 1949-2553 (Linking)
VI  - 8
IP  - 6
DP  - 2017 Feb 7
TI  - Elevated plasma interleukin-37 playing an important role in acute coronary 
      syndrome through suppression of ROCK activation.
PG  - 9686-9695
LID - 10.18632/oncotarget.14195 [doi]
AB  - OBJECTIVE: The plasma level of interleukin-37 is elevated in patients with acute 
      coronary syndrome, however, its function during the onset and progress of the 
      disease remains unclear. This study aimed to investigate the clinical 
      significance of IL-37 in acute coronary syndrome and its underlying mechanism. 
      METHODS: 124 patients with acute coronary syndrome and 40 healthy controls were 
      recruited in this study. Plasma interleukin-37 levels were measured in 41 
      patients with ST elevation myocardial infarction (STEMI), 41 patients with 
      non-STEMI, 42 patients with unstable angina, and 40 controls. Mortality was 
      defined as an event. RESULTS: In this study, the mean follow-up period was 
      824+/-306 days (2-1077 days). 22% (n=27) of patients died. The mortality rate was 
      significantly lower in patients with interleukin-37 serum levels below the median 
      (6.4 pg/mL) than those with interleukin-37 serum levels above 6.4 pg/mL at 
      36-month follow-up (16% vs. 24%, p=0.02, log rank X2=5.39). Highly concentration 
      of the anti-inflammatory interleukin-37 exerted a protective effect by 
      suppressing the activated Rho Kinase (ROCK) activity in the peripheral blood 
      mononuclear cells in vivo and in vitro after ischemia/reperfusion injury and 
      stimulation of the Rho activator, calpeptin. CONCLUSIONS: The interleukin-37 
      level is significantly increased in acute coronary syndrome. Elevated baseline 
      interleukin-37 levels in patients on admission are associated with poor outcomes. 
      Thus, we propose that interleukin-37 could be a biomarker predictive of mortality 
      in acute coronary syndrome. Moreover, this study reveals that the protective 
      effect of interleukin-37 against atherosclerosis may involve the inhibition of 
      ROCK activity.
FAU - Yang, Tengyu
AU  - Yang T
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Fang, Fang
AU  - Fang F
AD  - Division of cardiology, Department of Medicine and Therapeutics, Prince of Wales 
      Hospital, Li Ka Shing Institute of Health and Sciences, Institute of Vascular 
      Medicine, The Chinese University of Hong Kong, Hong Kong, China.
FAU - Chen, Yawen
AU  - Chen Y
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Ma, Jing
AU  - Ma J
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Xiao, Zhaowen
AU  - Xiao Z
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Zou, Songfeng
AU  - Zou S
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Zheng, Na
AU  - Zheng N
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Yan, Dewen
AU  - Yan D
AD  - Department of Endocrinology, The First Affiliated Hospital of Shenzhen 
      University, Shenzhen, China.
FAU - Liao, Songyan
AU  - Liao S
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Chen, Shaoyuan
AU  - Chen S
AD  - Cardiology Division, Department of Medicine, The Nanshan Hostipal, Shenzhen, 
      Guangdong, China.
FAU - Fang, Hongchen
AU  - Fang H
AD  - Cardiology Division, Department of Medicine, The Nanshan Hostipal, Shenzhen, 
      Guangdong, China.
FAU - Yu, Chekmen
AU  - Yu C
AD  - Division of cardiology, Department of Medicine and Therapeutics, Prince of Wales 
      Hospital, Li Ka Shing Institute of Health and Sciences, Institute of Vascular 
      Medicine, The Chinese University of Hong Kong, Hong Kong, China.
FAU - Liu, Jie
AU  - Liu J
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
FAU - Dong, Ming
AU  - Dong M
AD  - Division of Pathophysiology, Medical College, Shenzhen University, Shenzhen, 
      Guangdong, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Oncotarget
JT  - Oncotarget
JID - 101532965
RN  - 0 (Biomarkers)
RN  - 0 (Dipeptides)
RN  - 0 (Enzyme Activators)
RN  - 0 (IL37 protein, human)
RN  - 0 (Interleukin-1)
RN  - 18X9FR245W (calpeptin)
RN  - EC 2.7.11.1 (rho-Associated Kinases)
SB  - IM
MH  - Acute Coronary Syndrome/*blood/diagnosis/enzymology/mortality
MH  - Aged
MH  - Aged, 80 and over
MH  - Biomarkers/blood
MH  - Case-Control Studies
MH  - Cells, Cultured
MH  - Chi-Square Distribution
MH  - Dipeptides/pharmacology
MH  - Enzyme Activation
MH  - Enzyme Activators/pharmacology
MH  - Female
MH  - Humans
MH  - Interleukin-1/*blood
MH  - Leukocytes, Mononuclear/drug effects/*enzymology
MH  - Male
MH  - Middle Aged
MH  - Non-ST Elevated Myocardial Infarction/*blood/diagnosis/enzymology/mortality
MH  - Prognosis
MH  - Risk Factors
MH  - ST Elevation Myocardial Infarction/*blood/diagnosis/enzymology/mortality
MH  - Time Factors
MH  - Up-Regulation
MH  - rho-Associated Kinases/*metabolism
PMC - PMC5354763
OTO - NOTNLM
OT  - ROCK activity
OT  - acute coronary syndrome
OT  - interleukin -37
COIS- CONFLICTS OF INTEREST The authors declare no conflicts of interest.
EDAT- 2017/01/01 06:00
MHDA- 2018/02/23 06:00
PMCR- 2017/02/07
CRDT- 2017/01/01 06:00
PHST- 2016/10/15 00:00 [received]
PHST- 2016/11/24 00:00 [accepted]
PHST- 2017/01/01 06:00 [pubmed]
PHST- 2018/02/23 06:00 [medline]
PHST- 2017/01/01 06:00 [entrez]
PHST- 2017/02/07 00:00 [pmc-release]
AID - 14195 [pii]
AID - 10.18632/oncotarget.14195 [doi]
PST - ppublish
SO  - Oncotarget. 2017 Feb 7;8(6):9686-9695. doi: 10.18632/oncotarget.14195.