PMID- 33488923
OWN - NLM
STAT- MEDLINE
DCOM- 20210903
LR  - 20210903
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2020
DP  - 2020
TI  - NAMPT/SIRT1 Attenuate Ang II-Induced Vascular Remodeling and Vulnerability to 
      Hypertension by Inhibiting the ROS/MAPK Pathway.
PG  - 1974265
LID - 10.1155/2020/1974265 [doi]
LID - 1974265
AB  - Hypertension is characterized by endothelial dysfunction, vascular remodeling, 
      and rearrangement of the extracellular matrix. Besides, the pathogenesis of 
      hypertension is closely related to excess generation of reactive oxygen species 
      (ROS). Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme 
      in nicotinamide adenine dinucleotide (NAD) biosynthesis that influences the 
      activity of NAD-dependent enzymes, such as sirtuins, which possess NAD-dependent 
      protein deacetylase activity and cleave NAD during the deacetylation cycle. 
      Recently, NAMPT has been shown to play a crucial role in various diseases 
      associated with oxidative stress. However, the function and regulation of NAMPT 
      in hypertension have not been extensively explored. In the present study, we 
      identified NAMPT as a crucial regulator of hypertension, because NAMPT expression 
      was significantly downregulated in both patients with hypertension and 
      experimental animals. NAMPT knockout (NAMPT+/-) mice exhibited a significantly 
      higher blood pressure and ROS levels after stimulation with angiotensin II (Ang 
      II) than wild-type mice, and the administration of recombinant human NAMPT 
      (rhNAMPT) reversed this effect. In vivo, overexpression of NAMPT protected 
      against angiotensin II- (Ang II-) induced hypertension by inhibiting ROS 
      production via sirtuin 1 in mouse aortic endothelial cells (MAECs) and mouse 
      aortic vascular smooth muscle cells (MOVAs). In turn, NAMPT alleviated the 
      ROS-induced mitogen-activated protein kinase (MAPK) pathway. In conclusion, NAMPT 
      might be a novel biomarker and a therapeutic target in hypertension.
CI  - Copyright (c) 2020 Lei Zhou et al.
FAU - Zhou, Lei
AU  - Zhou L
AUID- ORCID: 0000-0003-0917-9986
AD  - Department of Cardiothoracic Surgery, Tongji Hospital, School of Medicine, Tongji 
      University, Shanghai 200065, China.
FAU - Zhang, Sheng
AU  - Zhang S
AUID- ORCID: 0000-0002-7859-6487
AD  - Department of Cardiology, East Hospital, School of Medicine, Tongji University, 
      310000, China.
FAU - Bolor-Erdene, Enkhbat
AU  - Bolor-Erdene E
AUID- ORCID: 0000-0001-6295-481X
AD  - Department of Cardiothoracic Surgery, Tongji Hospital, School of Medicine, Tongji 
      University, Shanghai 200065, China.
FAU - Wang, Lingwei
AU  - Wang L
AUID- ORCID: 0000-0001-8090-3645
AD  - Department of Thoracic Surgery, East Hospital, School of Medicine, Tongji 
      University, Shanghai 310000, China.
FAU - Tian, Ding
AU  - Tian D
AUID- ORCID: 0000-0002-1104-8101
AD  - Department of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong 
      University, Shanghai 200092, China.
FAU - Mei, Yunqing
AU  - Mei Y
AUID- ORCID: 0000-0002-5269-2067
AD  - Department of Cardiothoracic Surgery, Tongji Hospital, School of Medicine, Tongji 
      University, Shanghai 200065, China.
LA  - eng
PT  - Journal Article
DEP - 20201230
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (Reactive Oxygen Species)
RN  - 11128-99-7 (Angiotensin II)
RN  - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.5.1.- (Sirtuin 1)
SB  - IM
MH  - Angiotensin II/*toxicity
MH  - Animals
MH  - Case-Control Studies
MH  - Female
MH  - Humans
MH  - Hypertension/etiology/metabolism/pathology/*prevention & control
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Middle Aged
MH  - Mitogen-Activated Protein Kinases/*antagonists & inhibitors/genetics/metabolism
MH  - Myocytes, Smooth Muscle/drug effects/metabolism/pathology
MH  - Nicotinamide Phosphoribosyltransferase/genetics/*metabolism
MH  - Oxidative Stress
MH  - Reactive Oxygen Species/*metabolism
MH  - Signal Transduction
MH  - Sirtuin 1/genetics/*metabolism
MH  - *Vascular Remodeling
PMC - PMC7791967
COIS- The authors have no conflicts of interest to declare.
EDAT- 2021/01/26 06:00
MHDA- 2021/09/04 06:00
PMCR- 2020/12/30
CRDT- 2021/01/25 05:40
PHST- 2020/07/04 00:00 [received]
PHST- 2020/11/24 00:00 [revised]
PHST- 2020/12/07 00:00 [accepted]
PHST- 2021/01/25 05:40 [entrez]
PHST- 2021/01/26 06:00 [pubmed]
PHST- 2021/09/04 06:00 [medline]
PHST- 2020/12/30 00:00 [pmc-release]
AID - 10.1155/2020/1974265 [doi]
PST - epublish
SO  - Oxid Med Cell Longev. 2020 Dec 30;2020:1974265. doi: 10.1155/2020/1974265. 
      eCollection 2020.