Evidence map›Paper›PMID 33627622›Full record

ArticleCell death & disease2021

Oxidative stress-induced mitophagy is suppressed by the miR-106b-93-25 cluster in a protective manner.

Cheng Zhang, Pengqing Nie, Chunliu Zhou, Yue Hu, Suling Duan, Meijia Gu, Dongxu Jiang, Yunfu Wang, Zixin Deng, Jincao Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-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

34 citing papers in PubMed, 44 citations in OpenAlex.

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  17. The Role of Sirtuins in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2023
    Review
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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

12 authors at 3 institutions in 1 country.

Cheng ZhangKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Pengqing NieKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Chunliu ZhouKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Yue HuKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Suling DuanKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Meijia GuKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Dongxu JiangKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Yunfu WangTaihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.
Zixin DengKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.
Jincao ChenBrain Center, Department of Neurosurgery, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Shi ChenKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China.ORCID 0000-0002-8965-1015
Lianrong WangKey Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences, Wuhan University, Wuhan, 430071, Hubei, China. lianrong@whu.edu.cn.ORCID 0000-0003-1669-6340
Wuhan University · CNHubei University of Medicine · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased reactive oxygen species levels in the mitochondrial matrix can induce Parkin-dependent mitophagy, which selectively degrades dysfunctional mitochondria via the autolysosome pathway. Phosphorylated mitofusin-2 (MFN2), a receptor of parkin RBR E3 ubiquitin-protein ligase (Parkin), interacts with Parkin to promote the ubiquitination of mitochondrial proteins; meanwhile, the mitophagy receptors Optineurin (OPTN) and nuclear dot protein 52 (NDP52) are recruited to damaged mitochondria to promote mitophagy. However, previous studies have not investigated changes in the levels of OPTN, MFN2, and NDP52 during Parkin-mediated mitophagy. Here, we show that mild and sustained hydrogen peroxide (H

Indexed as

MitophagyOxidative Stress3' Untranslated RegionsCell Cycle ProteinsGene Expression RegulationGlycogen Synthase Kinase 3 betaGTP PhosphohydrolasesHEK293 CellsHeLa CellsHumansHydrogen PeroxideMembrane Transport ProteinsMicroRNAsMitochondriaMitochondrial ProteinsNuclear Proteins3' Untranslated RegionsCALCOCO2 protein, humanCell Cycle ProteinsGlycogen Synthase Kinase 3 betaGSK3B protein, humanGTP PhosphohydrolasesHydrogen PeroxideMAS1 protein, humanMembrane Transport ProteinsMFN2 protein, humanMicroRNAsMIRN106 microRNA, humanMIRN25 microRNA, humanMIRN93 microRNA, humanMitochondrial ProteinsMYC protein, humanNuclear ProteinsOPTN protein, humanparkin proteinProto-Oncogene MasProto-Oncogene Proteins c-mycUbiquitin-Protein Ligases

Identifiers

PMID33627622
PMCPMC7904769
OpenAlexW3129935925

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.