PMID- 32526454
OWN - NLM
STAT- MEDLINE
DCOM- 20210226
LR  - 20210226
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 128
DP  - 2020 Aug
TI  - Oxygen homeostasis and cardiovascular disease: A role for HIF?
PG  - 110338
LID - S0753-3322(20)30531-X [pii]
LID - 10.1016/j.biopha.2020.110338 [doi]
AB  - Hypoxia, the decline of tissue oxygen stress, plays a role in mediating cellular 
      processes. Cardiovascular disease, relatively widespread with increased 
      mortality, is closely correlated with oxygen homeostasis regulation. Besides, 
      hypoxia-inducible factor-1(HIF-1) is reported to be a crucial component in 
      regulating systemic hypoxia-induced physiological and pathological modifications 
      like oxidative stress, damage, angiogenesis, vascular remodeling, inflammatory 
      reaction, and metabolic remodeling. In addition, HIF1 controls the movement, 
      proliferation, apoptosis, differentiation and activity of numerous core cells, 
      such as cardiomyocytes, endothelial cells (ECs), smooth muscle cells (SMCs), and 
      macrophages. Here we review the molecular regulation of HIF-1 in cardiovascular 
      diseases, intended to improve therapeutic approaches for clinical diagnoses. 
      Better knowledge of the oxygen balance control and the signal mechanisms involved 
      is important to advance the development of hypoxia-related diseases.
CI  - Copyright (c) 2020 The Author(s). Published by Elsevier Masson SAS.. All rights 
      reserved.
FAU - Li, Xinyu
AU  - Li X
AD  - Department of Pediatrics, The Third Xiangya Hospital, Central South University, 
      Changsha, Hunan Province 410013, China; Xiangya School of Medicine, Central South 
      University, Changsha, Hunan Province 410013, China.
FAU - Zhang, Quyan
AU  - Zhang Q
AD  - Department of Pediatrics, The Third Xiangya Hospital, Central South University, 
      Changsha, Hunan Province 410013, China; Xiangya School of Medicine, Central South 
      University, Changsha, Hunan Province 410013, China.
FAU - Nasser, M I
AU  - Nasser MI
AD  - Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, 
      Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510100, China.
FAU - Xu, Linyong
AU  - Xu L
AD  - Xiangya School of Life Science, Central South University, Changsha, Hunan 
      Province 410013, China.
FAU - Zhang, Xueyan
AU  - Zhang X
AD  - Department of Pediatrics, The Third Xiangya Hospital, Central South University, 
      Changsha, Hunan Province 410013, China; Xiangya School of Medicine, Central South 
      University, Changsha, Hunan Province 410013, China.
FAU - Zhu, Ping
AU  - Zhu P
AD  - Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, 
      Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510100, China. 
      Electronic address: tanganqier@163.com.
FAU - He, Qingnan
AU  - He Q
AD  - Department of Pediatrics, The Third Xiangya Hospital, Central South University, 
      Changsha, Hunan Province 410013, China. Electronic address: heqn2629@163.com.
FAU - Zhao, Mingyi
AU  - Zhao M
AD  - Department of Pediatrics, The Third Xiangya Hospital, Central South University, 
      Changsha, Hunan Province 410013, China. Electronic address: 36163773@qq.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200608
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 0 (Reactive Oxygen Species)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/*metabolism/pathology/physiopathology
MH  - Cardiovascular System/*metabolism/pathology/physiopathology
MH  - Homeostasis
MH  - Humans
MH  - Hypoxia/*metabolism/pathology/physiopathology
MH  - Hypoxia-Inducible Factor 1/*metabolism
MH  - Oxidative Stress
MH  - Oxygen/*metabolism
MH  - Reactive Oxygen Species/metabolism
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Blood vessels
OT  - Cardiovascular diseases
OT  - Hypoxia-Inducible factor 1
OT  - Macrophages
OT  - Myocardial infarction
COIS- Declaration of Competing Interest The authors declare no conflict of interest.
EDAT- 2020/06/12 06:00
MHDA- 2021/02/27 06:00
CRDT- 2020/06/12 06:00
PHST- 2020/03/28 00:00 [received]
PHST- 2020/05/27 00:00 [revised]
PHST- 2020/05/30 00:00 [accepted]
PHST- 2020/06/12 06:00 [pubmed]
PHST- 2021/02/27 06:00 [medline]
PHST- 2020/06/12 06:00 [entrez]
AID - S0753-3322(20)30531-X [pii]
AID - 10.1016/j.biopha.2020.110338 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2020 Aug;128:110338. doi: 10.1016/j.biopha.2020.110338. Epub 
      2020 Jun 8.