Evidence map›Paper›PMID 29367621›Full record

ArticleCell death & disease2018

Optineurin-mediated mitophagy protects renal tubular epithelial cells against accelerated senescence in diabetic nephropathy.

Kehong Chen, Huanzi Dai, Junjie Yuan, Jia Chen, Lirong Lin, Weiwei Zhang, Limin Wang, Jianguo Zhang, Kailong Li, Yani He

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

97 citing papers in PubMed, 142 citations in OpenAlex.

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  19. Autophagy and Mitophagy in Diabetic Kidney Disease-A Literature Review.International journal of molecular sciences · 2025
    Review
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37 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Kehong ChenDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Huanzi DaiDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Junjie YuanDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Jia ChenDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Lirong LinDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Weiwei ZhangDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Limin WangDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Jianguo ZhangDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Kailong LiDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.
Yani HeDepartment of Nephrology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing, PR China. heynmail@yahoo.com.
Army Medical University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Premature senescence is a key process in the progression of diabetic nephropathy (DN). Premature senescence of renal tubular epithelial cells (RTEC) in DN may result from the accumulation of damaged mitochondria. Mitophagy is the principal process that eliminates damaged mitochondria through PTEN-induced putative kinase 1 (PINK1)-mediated recruitment of optineurin (OPTN) to mitochondria. We aimed to examine the involvement of OPTN in mitophagy regulation of cellular senescence in RTEC in the context of DN. In vitro, the expression of senescence markers P16, P21, DcR2, SA-β-gal, SAHF, and insufficient mitophagic degradation marker (mitochondrial P62) in mouse RTECs increased after culture in 30 mM high-glucose (HG) conditions for 48 h. Mitochondrial fission/mitophagy inhibitor Mdivi-1 significantly enhanced RTEC senescence under HG conditions, whereas autophagy/mitophagy agonist Torin1 inhibited cell senescence. MitoTempo inhibited HG-induced mitochondrial reactive oxygen species and cell senescence with or without Mdivi-1. The expression of PINK1 and OPTN, two regulatory factors for mitophagosome formation, decreased significantly after HG stimulation. Overexpression of PINK1 did not enhance mitophagosome formation under HG conditions. OPTN silencing significantly inhibited HG-induced mitophagosome formation, and overexpression of OPTN relieved cellular senescence through promoting mitophagy. In clinical specimens, renal OPTN expression was gradually decreased with increased tubulointerstitial injury scores. OPTN-positive renal tubular cells did not express senescence marker P16. OPTN expression also negatively correlated with serum creatinine levels, and positively correlated with eGFR. Thus, OPTN-mediated mitophagy plays a crucial regulatory role in HG-induced RTEC senescence in DN. OPTN may, therefore, be a potential antisenescence factor in DN.

Indexed as

Cellular SenescenceCytoprotectionMitophagyAnimalsCell Cycle ProteinsDiabetic NephropathiesDisease ProgressionEpithelial CellsEye ProteinsGlucoseHumansKidney TubulesMembrane Transport ProteinsMice, Inbred C57BLMitochondriaPhagosomesCell Cycle ProteinsEye ProteinsGlucoseMembrane Transport ProteinsOPTN protein, humanOptn protein, mouseProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesTranscription Factor TFIIIA

Identifiers

PMID29367621
PMCPMC5833650
OpenAlexW2791218358

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.