Evidence map›Paper›PMID 39467886›Full record

ArticleCardiovascular toxicology2025

Inhibition of CB1R in the Hypothalamic Paraventricular Nucleus Ameliorates Hypertension Through Wnt/β-Catenin/RAS Pathway.

Hong-Li Gao, Yu Yang, Hua Tian, Li-Yan Fu, Kai-Li Liu, Xiu-Yue Jia, Xiao-Lian Shi, Yu-Ming Kang, Xiao-Jing Yu

Abstract read
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In one paragraph

Article in Cardiovascular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
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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

9 authors.

Hong-Li Gao *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Yu Yang *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Hua TianDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Li-Yan FuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Kai-Li LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Xiu-Yue JiaDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Xiao-Lian ShiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Yu-Ming KangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China. ykang@mail.xjtu.edu.cn.
Xiao-Jing YuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University Health Science Center, Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China. yuxiaojing@mail.xjtu.edu.cn.

Funding

China Postdoctoral Science Foundation 2023M742801National Natural Science Foundation of China 82070440National Natural Science Foundation of China 82200473National Natural Science Foundation of China 82270468Natural Science Basic Research Program of Shaanxi Province 2024JC-YBMS-764Project supported by the Open Fund for Key Laboratory of precision medicine for children's diseases in Shaanxi province KFJJ2023-01Shaanxi Province Postdoctoral Science Foundation 2023BSHYDZZ01
6 · The paper itself

Abstract

The hypothalamic paraventricular nucleus (PVN), as an important integrating center, plays a prominent role in the pathogenesis of hypertension, in maintaining the stability of cardiovascular activity through peripheral sympathetic nervous activity and secretion of various humoral factors. Acknowledging that the mechanistic targets of the endocannabinoid type 1 receptor (CB1R) are the key signaling systems involved in the regulation of hypertension, we sought to clarify whether inhibition of CB1R within the PVN ameliorates hypertension through Wnt/β-catenin/RAS pathway. Spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats were randomly assigned to different groups and treated with bilateral PVN injections of AM251 (CB1R antagonist, 10 µg/h) or vehicle (artificial cerebrospinal fluid, aCSF) for four weeks. Bilateral PVN injections of AM251 significantly decreased the heart rate, the body weight and the mean arterial pressure in SHRs. AM251 lowered the expression of CB1R, Wnt3, active-β-catenin, p-IKKβ, RAS components, pro-inflammatory cytokines and elevated the expression level of Glycogen synthase kinase3β and Superoxide Dismutase in the PVN of hypertensive rats. Our findings suggest that inhibition of CB1R in the PVN ameliorates hypertension through Wnt/β-catenin/RAS pathway and broaden our current understanding of the pathological mechanism and clinical treatment of hypertension.

Indexed as

Antihypertensive AgentsArterial Pressurebeta CateninCannabinoid Receptor AntagonistsHypertensionParaventricular Hypothalamic NucleusPiperidinesPyrazolesReceptor, Cannabinoid, CB1Renin-Angiotensin SystemWnt Signaling PathwayAnimalsCytokinesDisease Models, AnimalGlycogen Synthase Kinase 3 betaInflammation MediatorsAM 251Antihypertensive Agentsbeta CateninCannabinoid Receptor AntagonistsCtnnb1 protein, ratCytokinesGlycogen Synthase Kinase 3 betaGsk3b protein, ratInflammation MediatorsPiperidinesPyrazolesReceptor, Cannabinoid, CB1Superoxide DismutaseEndocannabinoid type 1 receptorHypertensionHypothalamic paraventricular nucleusSympathetic nervous activityWnt/β-catenin/RAS pathway

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Registered trials

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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.