Evidence map›Paper›PMID 31210840›Full record

ArticleOxidative medicine and cellular longevity2019

NADPH Oxidase Hyperactivity Contributes to Cardiac Dysfunction and Apoptosis in Rats with Severe Experimental Pancreatitis through ROS-Mediated MAPK Signaling Pathway.

Yi Wen, Ruohong Liu, Ning Lin, Hao Luo, Jiajia Tang, Qilin Huang, Hongyu Sun, Lijun Tang

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. 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
6.8field-weighted citation impact, top 3% 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, 52 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

8 authors at 3 institutions in 1 country.

Yi WenDepartment of Graduate School, The Third Military Medical University (Army Medical University), Chongqing, China.
Ruohong LiuDepartment of Graduate School, The Third Military Medical University (Army Medical University), Chongqing, China.
Ning LinDepartment of General Surgery & Pancreatic Injury and Repair Key Laboratory of Sichuan Province, The General Hospital of Western Theater Command (Chengdu Military General Hospital), Chengdu, China.
Hao LuoDepartment of General Surgery & Pancreatic Injury and Repair Key Laboratory of Sichuan Province, The General Hospital of Western Theater Command (Chengdu Military General Hospital), Chengdu, China.
Jiajia TangDepartment of Ultrasound, Chinese Academy of Medical Sciences and Peking Union Medical College Hospital, Beijing, China.
Qilin HuangDepartment of General Surgery & Pancreatic Injury and Repair Key Laboratory of Sichuan Province, The General Hospital of Western Theater Command (Chengdu Military General Hospital), Chengdu, China.
Hongyu SunDepartment of General Surgery & Pancreatic Injury and Repair Key Laboratory of Sichuan Province, The General Hospital of Western Theater Command (Chengdu Military General Hospital), Chengdu, China.ORCID 0000-0002-8587-0499
Lijun TangDepartment of Graduate School, The Third Military Medical University (Army Medical University), Chongqing, China.ORCID 0000-0001-6000-9515
Chengdu Military General Hospital · CNArmy Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NADPH oxidase (Nox) is considered a major source of reactive oxygen species (ROS) in the heart in normal and pathological conditions. However, the role of Nox in severe acute pancreatitis- (SAP-) associated cardiac injury remains unclear. Therefore, we aim to investigate the contribution of Nox to SAP-associated cardiac injury and to explore the underlying molecular mechanisms. Apocynin, a Nox inhibitor, was given at 20 mg/kg for 30 min before SAP induction by a retrograde pancreatic duct injection of 5% sodium taurocholate. Histopathological staining, Nox activity and protein expression, oxidative stress markers, apoptosis and associated proteins, cardiac-related enzyme indexes, and cardiac function were assessed in the myocardium in SAP rats. The redox-sensitive MAPK signaling molecules were also examined by western blotting. SAP rats exhibited significant cardiac impairment along with increased Nox activity and protein expression, ROS production, cell apoptosis, and proapoptotic Bax and cleaved caspase-3 protein levels. Notably, Nox inhibition with apocynin prevented SAP-associated cardiac injury evidenced by a decreased histopathologic score, cardiac-related enzymes, and cardiac function through the reduction of ROS production and cell apoptosis. This protective role was further confirmed by a simulation experiment

Indexed as

ApoptosisGene Expression Regulation, EnzymologicAnimalsbcl-2-Associated X ProteinCaspase 3Disease Models, AnimalHeart DiseasesMaleMAP Kinase Signaling SystemMyocardiumNADPH OxidasesPancreatitisRatsReactive Oxygen SpeciesSeverity of Illness IndexBax protein, ratbcl-2-Associated X ProteinCasp3 protein, ratCaspase 3NADPH OxidasesReactive Oxygen Species

Identifiers

PMID31210840
PMCPMC6532283
OpenAlexW2943835981

What OpenQuestion holds

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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.