Evidence map›Paper›PMID 31442911›Full record

ArticleRedox biology2019

Serum response factor (SRF) promotes ROS generation and hepatic stellate cell activation by epigenetically stimulating NCF1/2 transcription.

Ming Kong, Xuyang Chen, Fangqiao Lv, Haozhen Ren, Zhiwen Fan, Hao Qin, Liming Yu, Xiaolei Shi, Yong Xu

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 75 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

9 authors at 3 institutions in 1 country.

Ming KongKey Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Pathophysiology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Xuyang ChenKey Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Pathophysiology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Fangqiao LvDepartment of Cell Biology and the Municipal Laboratory of Liver Protection and Regulation of Regeneration, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Haozhen RenDepartment of Hepato-biliary Surgery and Department of Pathology, Affiliated Nanjing Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
Zhiwen FanDepartment of Hepato-biliary Surgery and Department of Pathology, Affiliated Nanjing Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
Hao QinKey Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Pathophysiology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Liming YuKey Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Pathophysiology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Xiaolei ShiDepartment of Hepato-biliary Surgery and Department of Pathology, Affiliated Nanjing Drum Tower Hospital of Nanjing University Medical School, Nanjing, China. Electronic address: njsxl2000@163.com.
Yong XuKey Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Department of Pathophysiology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China; Institute of Biomedical Research, Liaocheng University, Liaocheng, China. Electronic address: yjxu@njmu.edu.cn.
Nanjing Medical University · CNNanjing Drum Tower Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of hepatic stellate cells (HSC) is a hallmark event in liver fibrosis. Accumulation of reactive oxygen species (ROS) serves as a driving force for HSC activation. The regulatory subunits of the NOX complex, NCF1 (p47

Indexed as

Epigenesis, GeneticGene Expression RegulationTranscriptional ActivationAnimalsDisease SusceptibilityHepatic Stellate CellsLiver CirrhosisMiceMice, TransgenicModels, BiologicalNADPH OxidasesReactive Oxygen SpeciesSerum Response FactorNADPH OxidasesNcf2 protein, mouseneutrophil cytosolic factor 1Reactive Oxygen SpeciesSerum Response FactorHepatic stellate cellLiver fibrosisNeutrophil cytosolic factorReactive oxygen speciesSerum response factorTranscriptional regulation

Identifiers

PMID31442911
PMCPMC6831835
OpenAlexW2967546593

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.