Evidence map›Paper›PMID 38173512›Full record

ArticleHeliyon2024

VDAC1, as a downstream molecule of MLKL, participates in OGD/R-induced necroptosis by inducing mitochondrial damage.

Hao Wan, Yan-di Yang, Qi Zhang, Yu-Hua Chen, Xi-Min Hu, Yan-Xia Huang, Lei Shang, Kun Xiong

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2024. 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
3.2field-weighted citation impact, top 8% 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, 21 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 2 institutions in 1 country.

Hao WanDepartment of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.
Yan-di YangDepartment of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.
Qi ZhangDepartment of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.
Yu-Hua ChenDepartment of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.
Xi-Min HuDepartment of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.
Yan-Xia HuangDepartment of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.
Lei ShangJiangxi Research Institute of Ophthalmology and Visual Sciences, Affiliated Eye Hospital of Nanchang University, Nanchang, China.
Kun XiongDepartment of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, China.
Central South University · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion (I/R) injury constitutes a significant risk factor for a range of diseases, including ischemic stroke, myocardial infarction, and trauma. Following the restoration of blood flow post-tissue ischemia, oxidative stress can lead to various forms of cell death, including necrosis, apoptosis, autophagy, and necroptosis. Recent evidence has highlighted the crucial role of mitochondrial dysfunction in I/R injury. Nevertheless, there remains much to be explored regarding the molecular signaling network governing cell death under conditions of oxidative stress. Voltage-dependent anion channel 1 (VDAC1), a major component in the outer mitochondrial membrane, is closely involved in the regulation of cell death. In a cellular model of oxygen-glucose deprivation and reoxygenation (OGD/R), which effectively simulates I/R injury

Indexed as

Mitochondria damageMLKLNecroptosisOGD/RVDAC1

Identifiers

PMID38173512
PMCPMC10761567
OpenAlexW4389542138

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.