PMID- 31853248
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220411
IS  - 1671-5411 (Print)
IS  - 1671-5411 (Linking)
VI  - 16
IP  - 11
DP  - 2019 Nov
TI  - Endogenous hydrogen sulfide and ERK1/2-STAT3 signaling pathway may participate in 
      the association between homocysteine and hypertension.
PG  - 822-834
LID - 10.11909/j.issn.1671-5411.2019.11.007 [doi]
AB  - BACKGROUND: Homocysteine (Hcy) is a risk factor for hypertension, although the 
      mechanisms are poorly understood. METHODS: We first explored the relationship 
      between Hcy levels and blood pressure (BP) by analyzing the clinical data of 
      primary hypertensive patients admitted to our hospital. Secondly, we explored a 
      rat model to study the effect of Hcy on blood pressure and the role of H(2)S. An 
      hyperhomocysteinemia (HHcy) rat model was induced to explore the effect of Hcy on 
      blood pressure and the possible mechanism. We carried out tissue histology, 
      extraction and examination of RNA and protein. Finally, we conducted cell 
      experiments to determine a likely mechanism through renin-angiotensin-aldosterone 
      system (RAAS) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling 
      pathway. RESULTS: In primary hypertensive inpatients with HHcy, blood pressure 
      was significantly higher as compared with inpatient counterparts lacking HHcy. In 
      the rat model, blood pressure of the Wistar rats was significantly increased with 
      increases in serum Hcy levels and decreased after folate treatment. Angiotensin 
      converting enzyme 1 (ACE1) expression in the Wistar Hcy group was enhanced 
      comparing to controls, but was decreased in the Wistar folate group. Angiotensin 
      II receptor type 1 (AGTR1) levels in the kidney tissue increased in the Wistar 
      folate group. Both serum H(2)S and kidney cystathionine gamma-lyase decreased with 
      elevated levels of serum Hcy. In vitro, increased concentrations and treatment 
      times for Hcy were associated with increased expression of collagen type 1 and 
      AGTR1. This dose and time dependent response was also observed for p-STAT3 and 
      p-ERK1/2 expression. CONCLUSION: Endogenous H(2)S might mediate the process of 
      altered blood pressure in response to changes in serum Hcy levels, in a process 
      that is partly dependent on activated RAAS and ERK1/2-STAT3 signaling pathway.
CI  - Institute of Geriatric Cardiology.
FAU - Shi, Lin
AU  - Shi L
AD  - Hypertension Research Laboratory, Department of Cardiology, Peking University 
      People's Hospital, Beijing, China.
FAU - Liu, Xiao-Yun
AU  - Liu XY
AD  - Hypertension Research Laboratory, Department of Cardiology, Peking University 
      People's Hospital, Beijing, China.
FAU - Huang, Zhi-Gang
AU  - Huang ZG
AD  - Hypertension Research Laboratory, Department of Cardiology, Peking University 
      People's Hospital, Beijing, China.
AD  - Emergency Department, Peking University Shenzhen Hospital, Shenzhen, China.
FAU - Ma, Zhi-Yi
AU  - Ma ZY
AD  - Hypertension Research Laboratory, Department of Cardiology, Peking University 
      People's Hospital, Beijing, China.
FAU - Xi, Yang
AU  - Xi Y
AD  - Hypertension Research Laboratory, Department of Cardiology, Peking University 
      People's Hospital, Beijing, China.
FAU - Wang, Lu-Yan
AU  - Wang LY
AD  - Hypertension Research Laboratory, Department of Cardiology, Peking University 
      People's Hospital, Beijing, China.
FAU - Sun, Ning-Ling
AU  - Sun NL
AD  - Hypertension Research Laboratory, Department of Cardiology, Peking University 
      People's Hospital, Beijing, China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - J Geriatr Cardiol
JT  - Journal of geriatric cardiology : JGC
JID - 101237881
PMC - PMC6911803
OTO - NOTNLM
OT  - Angiotensin converting enzyme 1
OT  - Blood pressure
OT  - ERK1/2-STAT3 signaling pathway
OT  - Homocysteine
OT  - Hydrogen sulfide
EDAT- 2019/12/20 06:00
MHDA- 2019/12/20 06:01
PMCR- 2019/11/01
CRDT- 2019/12/20 06:00
PHST- 2019/12/20 06:00 [entrez]
PHST- 2019/12/20 06:00 [pubmed]
PHST- 2019/12/20 06:01 [medline]
PHST- 2019/11/01 00:00 [pmc-release]
AID - jgc-16-11-822 [pii]
AID - 10.11909/j.issn.1671-5411.2019.11.007 [doi]
PST - ppublish
SO  - J Geriatr Cardiol. 2019 Nov;16(11):822-834. doi: 
      10.11909/j.issn.1671-5411.2019.11.007.