Evidence map›Paper›PMID 32817651›Full record

ArticlePLoS biology2020

Klf5 down-regulation induces vascular senescence through eIF5a depletion and mitochondrial fission.

Dong Ma, Bin Zheng, He-Liang Liu, Yong-Bo Zhao, Xiao Liu, Xin-Hua Zhang, Qiang Li, Wei-Bo Shi, Toru Suzuki, Jin-Kun Wen

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.7field-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

43 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
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  4. Ythdc1-p300-Klf5 Complex-Mediated Golgi Dysfunction Promotes Aortic Aneurysm.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  16. NAging and disease · 2024
    Review
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  18. Review
  19. Article
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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

10 authors at 3 institutions in 2 countries.

Dong MaDepartment of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, China.ORCID 0000-0001-8288-4775
Bin ZhengDepartment of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, China.
He-Liang LiuSchool of Public Health, North China University of Science and Technology, Tangshan, China.
Yong-Bo ZhaoDepartment of Cardiac surgery, the Fourth Hospital of Hebei Medical University, Shi Jiazhuang, China.
Xiao LiuDepartment of Cardiac surgery, the Fourth Hospital of Hebei Medical University, Shi Jiazhuang, China.
Xin-Hua ZhangDepartment of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, China.
Qiang LiDepartment of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, China.
Wei-Bo ShiDepartment of Forensic Medicine, Hebei Medical University, Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Shijiazhuang, China.
Toru SuzukiDepartment of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Jin-Kun WenDepartment of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, China.
Hebei Medical University · CNNorth China University of Science and Technology · CNUniversity of Leicester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although dysregulation of mitochondrial dynamics has been linked to cellular senescence, which contributes to advanced age-related disorders, it is unclear how Krüppel-like factor 5 (Klf5), an essential transcriptional factor of cardiovascular remodeling, mediates the link between mitochondrial dynamics and vascular smooth muscle cell (VSMC) senescence. Here, we show that Klf5 down-regulation in VSMCs is correlated with rupture of abdominal aortic aneurysm (AAA), an age-related vascular disease. Mice lacking Klf5 in VSMCs exacerbate vascular senescence and progression of angiotensin II (Ang II)-induced AAA by facilitating reactive oxygen species (ROS) formation. Klf5 knockdown enhances, while Klf5 overexpression suppresses mitochondrial fission. Mechanistically, Klf5 activates eukaryotic translation initiation factor 5a (eIF5a) transcription through binding to the promoter of eIF5a, which in turn preserves mitochondrial integrity by interacting with mitofusin 1 (Mfn1). Accordingly, decreased expression of eIF5a elicited by Klf5 down-regulation leads to mitochondrial fission and excessive ROS production. Inhibition of mitochondrial fission decreases ROS production and VSMC senescence. Our studies provide a potential therapeutic target for age-related vascular disorders.

Indexed as

AgedAngiotensin IIAnimalsAortaAortic Aneurysm, AbdominalCellular SenescenceEchocardiographyEndothelial CellsEukaryotic Translation Initiation Factor 5AFemaleGTP PhosphohydrolasesHumansKruppel-Like Transcription FactorsMaleMiceMice, KnockoutAngiotensin IIEukaryotic Translation Initiation Factor 5AGTP PhosphohydrolasesKlf5 protein, mouseKruppel-Like Transcription FactorsMfn1 protein, mousePeptide Initiation FactorsReactive Oxygen SpeciesRNA-Binding Proteins

Identifiers

PMID32817651
PMCPMC7462304
OpenAlexW3081161470

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.