Evidence map›Paper›PMID 32848742›Full record

ArticleFrontiers in pharmacology2020

Gallic Acid Attenuates Angiotensin II-Induced Hypertension and Vascular Dysfunction by Inhibiting the Degradation of Endothelial Nitric Oxide Synthase.

Xiao Yan, Qi-Yu Zhang, Yun-Long Zhang, Xiao Han, Shu-Bin Guo, Hui-Hua Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 50 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Xiao YanEmergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, and Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, China.
Qi-Yu ZhangDepartment of Cardiology, Institute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Yun-Long ZhangEmergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, and Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, China.
Xiao HanEmergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, and Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, China.
Shu-Bin GuoEmergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, and Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, China.
Hui-Hua LiEmergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, and Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, China.
Capital Medical University · CNBeijing Chao-Yang Hospital · CNDalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension is a major cause of heart attack and stroke. Our recent study revealed that gallic acid (GA) exerts protective effects on pressure overload-induced cardiac hypertrophy and dysfunction. However, the role of GA in angiotensin II (Ang II)-induced hypertension and vascular remodeling remains unknown. C57BL/6J mice were subjected to saline and Ang II infusion. Systolic blood pressure was measured using a tail-cuff system. Vascular remodeling and oxidative stress were examined by histopathological staining. Vasodilatory function was evaluated in the aortic ring. Our findings revealed that GA administration significantly ameliorated Ang II-induced hypertension, vascular inflammation, and fibrosis. GA also abolished vascular endothelial dysfunction and oxidative stress in Ang II-infused aortas. Mechanistically, GA treatment attenuated Ang II-induced upregulation of the immunoproteasome catalytic subunits β2i and β5i leading to reduction of the trypsin-like and chymotrypsin-like activity of the proteasome, which suppressed degradation of endothelial nitric oxide synthase (eNOS) and reduction of nitric oxide (NO) levels. Furthermore, blocking eNOS activity by using a specific inhibitor (

Indexed as

angiotensin IIeNOS degradationgallic acidhypertensionimmunoproteasome

Identifiers

PMID32848742
PMCPMC7396711
OpenAlexW3044688449

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.