Evidence map›Paper›PMID 34883403›Full record

ArticleRedox biology2021

RND3 attenuates oxidative stress and vascular remodeling in spontaneously hypertensive rat via inhibiting ROCK1 signaling.

Nan Wu, Fen Zheng, Na Li, Ying Han, Xiao-Qing Xiong, Jue-Jin Wang, Qi Chen, Yue-Hua Li, Guo-Qing Zhu, Ye-Bo Zhou

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  18. 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
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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

10 authors at 2 institutions in 1 country.

Nan WuKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Fen ZhengKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Na LiKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Ying HanKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Xiao-Qing XiongKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
Jue-Jin WangKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, 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 for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, China; Department of Pathophysiology, Nanjing Medical University, Nanjing, 211166, China. Electronic address: gqzhucn@njmu.edu.cn.
Ye-Bo ZhouKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, and Department of Physiology, Nanjing Medical University, Nanjing, 211166, China. Electronic address: zhouyebo666@njmu.edu.cn.
Nanjing Medical University · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Superoxide and vascular smooth muscle cells (VSMCs) migration and proliferation play crucial roles in the vascular remodeling. Vascular remodeling contributes to the development and complications of hypertension. Rho family GTPase 3 (RND3 or RhoE), an atypical small Rho-GTPase, is known to be involved in cancer development and metastasis. However, the roles of RND3 in superoxide production and cardiovascular remodeling are unknown. Here, we uncovered the critical roles of RND3 in attenuating superoxide production, VSMCs migration and proliferation, and vascular remodeling in hypertension and its underline mechanisms. VSMCs were isolated and prepared from thoracic aorta of Male Wistar-Kyoto rat (WKY) and spontaneously hypertensive rat (SHR). RND3 mRNA and protein expressions in arteries and VSMCs were down-regulated in SHR. RND3 overexpression in VSMCs reduced NAD(P)H oxidase (NOX) activity, NOX1 and NOX2 expressions, mitochondria superoxide generation, and H

Indexed as

HypertensionMigrationProliferationRND3SuperoxideVascular remodelingVascular smooth muscle cells

Identifiers

PMID34883403
PMCPMC8661704
OpenAlexW4200373402

What Socratic holds

Textmetadata
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 Socratic graph.