Evidence map›Paper›PMID 36293450›Full record

ArticleInternational journal of molecular sciences2022

Asprosin in the Paraventricular Nucleus Induces Sympathetic Activation and Pressor Responses via cAMP-Dependent ROS Production.

Xiao-Li Wang, Jing-Xiao Wang, Jun-Liu Chen, Wen-Yuan Hao, Wen-Zhou Xu, Zhi-Qin Xu, Yu-Tong Jiang, Pei-Qi Luo, Qi Chen, Yue-Hua Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Adipokine in Metabolic Liver Disease: Adipo-Brain-Liver Cross talk.International journal of endocrinology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. GLP-1 in the Hypothalamic Paraventricular Nucleus Promotes Sympathetic Activation and Hypertension.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  12. Article
  13. Article
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Xiao-Li WangKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing 211166, China.
Jing-Xiao WangKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing 211166, China.
Jun-Liu ChenKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing 211166, China.
Wen-Yuan HaoKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing 211166, China.
Wen-Zhou XuDepartment of Cardiology and Emergency Department, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China.
Zhi-Qin XuDepartment of Cardiology and Emergency Department, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China.
Yu-Tong JiangDepartment of Cardiology and Emergency Department, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China.
Pei-Qi LuoDepartment of Cardiology and Emergency Department, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China.
Qi ChenDepartment of Pathophysiology, Nanjing Medical University, Nanjing 211166, China.
Yue-Hua LiDepartment of Pathophysiology, Nanjing Medical University, Nanjing 211166, China.
Guo-Qing ZhuKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, Department of Physiology, Nanjing Medical University, Nanjing 211166, China.ORCID 0000-0002-3132-9592
Xiu-Zhen LiDepartment of Cardiology and Emergency Department, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, China.
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

National Natural Science Foundation of China 31871148 & 32071106
6 · The paper itself

Abstract

Asprosin is a newly discovered adipokine that is involved in regulating metabolism. Sympathetic overactivity contributes to the pathogenesis of several cardiovascular diseases. The paraventricular nucleus (PVN) of the hypothalamus plays a crucial role in the regulation of sympathetic outflow and blood pressure. This study was designed to determine the roles and underlying mechanisms of asprosin in the PVN in regulating sympathetic outflow and blood pressure. Experiments were carried out in male adult SD rats under anesthesia. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and heart rate (HR) were recorded, and PVN microinjections were performed bilaterally. Asprosin mRNA and protein expressions were high in the PVN. The high asprosin expression in the PVN was involved in both the parvocellular and magnocellular regions according to immunohistochemical analysis. Microinjection of asprosin into the PVN produced dose-related increases in RSNA, MAP, and HR, which were abolished by superoxide scavenger tempol, antioxidant N-acetylcysteine (NAC), and NADPH oxidase inhibitor apocynin. The asprosin promoted superoxide production and increased NADPH oxidase activity in the PVN. Furthermore, it increased the cAMP level, adenylyl cyclase (AC) activity, and protein kinase A (PKA) activity in the PVN. The roles of asprosin in increasing RSNA, MAP, and HR were prevented by pretreatment with AC inhibitor SQ22536 or PKA inhibitor H89 in the PVN. Microinjection of cAMP analog db-cAMP into the PVN played similar roles with asprosin in increasing the RSNA, MAP, and HR, but failed to further augment the effects of asprosin. Pretreatment with PVN microinjection of SQ22536 or H89 abolished the roles of asprosin in increasing superoxide production and NADPH oxidase activity in the PVN. These results indicated that asprosin in the PVN increased the sympathetic outflow, blood pressure, and heart rate via cAMP-PKA signaling-mediated NADPH oxidase activation and the subsequent superoxide production.

Indexed as

Paraventricular Hypothalamic NucleusSuperoxidesAcetylcysteineAdenylyl CyclasesAdipokinesAnimalsAntioxidantsBlood PressureCyclic AMP-Dependent Protein KinasesIsoquinolinesMaleNADPH OxidasesRatsRats, Sprague-DawleyReactive Oxygen SpeciesRNA, MessengerAcetylcysteineAdenylyl CyclasesAdipokinesAntioxidantsCyclic AMP-Dependent Protein KinasesIsoquinolinesN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamideNADPH OxidasesReactive Oxygen SpeciesRNA, MessengerSulfonamidesSuperoxidesasprosinblood pressureparaventricular nucleusreactive oxygen speciessympathetic activity

Identifiers

PMID36293450
PMCPMC9604496
OpenAlexW4306925919

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.