Evidence map›Paper›PMID 39113882›Full record

ArticleInternational journal of medical sciences2024

Roles and Mechanisms of Dopamine Receptor Signaling in Catecholamine Excess Induced Endothelial Dysfunctions.

Zhen Yang, Yingrui Li, Mengying Huang, Xin Li, Xuehui Fan, Chen Yan, Zenghui Meng, Bin Liao, Nazha Hamdani, Xiaoli Yang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of medical sciences, 2024. 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. Review
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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

13 authors.

Zhen YangDepartment of Ophthalmology, Affiliated Hospital of North Sichuan Medical College, 637000 Nanchong, Sichuan, China.
Yingrui LiFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Mengying HuangFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Xin LiFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Xuehui FanFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Chen YanFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Zenghui MengFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Bin LiaoDepartment of Cardiac Macrovascular Surgery, Affiliated Hospital of Southwest Medical University, 646000 Sichuan, China.
Nazha HamdaniDepartment of Cellular and Translational Physiology, Institute of Physiology, Ruhr University Bochum, 44801 Bochum, Germany and Institut für Forschung und Lehre (IFL), Molecular and Experimental Cardiology, Ruhr University Bochum, 44801 Bochum, Germany.
Xiaoli YangDepartment of Ophthalmology, Affiliated Hospital of North Sichuan Medical College, 637000 Nanchong, Sichuan, China.
Xiaobo ZhouFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Ibrahim El-BattrawyDepartment of Cellular and Translational Physiology, Institute of Physiology, Ruhr University Bochum, 44801 Bochum, Germany and Institut für Forschung und Lehre (IFL), Molecular and Experimental Cardiology, Ruhr University Bochum, 44801 Bochum, Germany.
Ibrahim AkinFirst Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction may contribute to pathogenesis of Takotsubo cardiomyopathy, but mechanism underlying endothelial dysfunction in the setting of catecholamine excess has not been clarified. The study reports that D1/D5 dopamine receptor signaling and small conductance calcium-activated potassium channels contribute to high concentration catecholamine induced endothelial cell dysfunction. For mimicking catecholamine excess, 100 μM epinephrine (Epi) was used to treat human cardiac microvascular endothelial cells. Patch clamp, FACS, ELISA, PCR, western blot and immunostaining analyses were performed in the study. Epi enhanced small conductance calcium-activated potassium channel current (I

Indexed as

Endothelial CellsEpinephrineReactive Oxygen SpeciesSignal TransductionCatecholaminesCyclic AMP-Dependent Protein KinasesEndothelium, VascularHumansNADPH OxidasesNitric OxideReceptors, DopamineReceptors, Dopamine D1Receptors, Dopamine D5Small-Conductance Calcium-Activated Potassium ChannelsCatecholaminesCyclic AMP-Dependent Protein KinasesEpinephrineNADPH OxidasesNitric OxideReactive Oxygen SpeciesReceptors, DopamineReceptors, Dopamine D1Receptors, Dopamine D5Small-Conductance Calcium-Activated Potassium Channelsdopamine receptorendothelial dysfunction, nitric oxide.small conductance calcium-activated potassium channelTakotsubo syndrome

Identifiers

PMID39113882
PMCPMC11302566

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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.