Evidence map›Paper›PMID 34609050›Full record

ArticleJournal of cellular and molecular medicine2021

Celecoxib reduces hepatic vascular resistance in portal hypertension by amelioration of endothelial oxidative stress.

Yang Tai, Chong Zhao, Linhao Zhang, Shihang Tang, Xintong Jia, Huan Tong, Rui Liu, Chengwei Tang, Jinhang Gao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. [Medical treatment of portal hypertensive bleeding in cirrhosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
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  10. Independent endothelial functions of PIEZO1 and TRPV4 in hepatic portal vein and predominance of PIEZO1 in mechanical and osmotic stress.Liver international : official journal of the International Association for the Study of the Liver · 2023
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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 at 1 institution in 1 country.

Yang TaiLaboratory of Gastroenterology and Hepatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Chong ZhaoLaboratory of Gastroenterology and Hepatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Linhao ZhangDepartment of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China.
Shihang TangDepartment of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China.
Xintong JiaDepartment of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China.
Huan TongDepartment of Gastroenterology, West China Hospital, Sichuan University, Chengdu, China.
Rui LiuLaboratory of Gastroenterology and Hepatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Chengwei TangLaboratory of Gastroenterology and Hepatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-2289-8240
Jinhang GaoLaboratory of Gastroenterology and Hepatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The balance between endothelial nitric oxide (NO) synthase (eNOS) activation and production of reactive oxygen species (ROS) is very important for NO homeostasis in liver sinusoidal endothelial cells (LSECs). Overexpression of cyclooxygenase-2 (COX-2), a major intravascular source of ROS production, has been observed in LSECs of cirrhotic liver. However, the links between low NO bioavailability and COX-2 overexpression in LSECs are unknown. This study has confirmed the link between low NO bioavailability and COX-2 overexpression by COX-2-dependent PGE2-EP2-ERK1/2-NOX1/NOX4 signalling pathway in LSECs in vivo and in vitro. In addition, the regulation of COX-2-independent LKB1-AMPK-NRF2-HO-1 signalling pathway on NO homeostasis in LSECs was also elucidated. The combinative effects of celecoxib on diminishment of ROS via COX-2-dependent and COX-2-independent signalling pathways greatly decreased NO scavenging. As a result, LSECs capillarisation was reduced, and endothelial dysfunction was corrected. Furthermore, portal hypertension of cirrhotic liver was ameliorated with substantial decreasing hepatic vascular resistance and great increase of portal blood flow. With the advance understanding of the mechanisms of LSECs protection, celecoxib may serve as a potential therapeutic candidate for patients with cirrhotic portal hypertension.

Indexed as

AnimalsAntioxidantsCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsDisease ManagementDisease Models, AnimalEndothelial CellsEndothelium, VascularGene Expression RegulationHeme Oxygenase (Decyclizing)HemodynamicsHepatic Stellate CellsHumansHypertension, PortalMaleAntioxidantsCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsHeme Oxygenase (Decyclizing)Hmox1 protein, ratNitric OxideReactive Oxygen Speciescyclooxygenase-2liver fibrosisliver sinusoidal endothelial cellsprostaglandinsreactive oxygen species

Identifiers

PMID34609050
PMCPMC8581330
OpenAlexW3204853831

What OpenQuestion holds

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LicenceCC BY
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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.