Evidence map›Paper›PMID 32687063›Full record

ArticleAging2020

SIRT1 alleviates high-magnitude compression-induced senescence in nucleus pulposus cells via PINK1-dependent mitophagy.

Yiyang Wang, Haoming Wang, Yunyun Zhuo, Yanzhu Hu, Zetong Zhang, Jixing Ye, Liehua Liu, Lei Luo, Chen Zhao, Qiang Zhou and 1 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.3field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 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

11 authors at 2 institutions in 1 country.

Yiyang WangDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Haoming WangTissue Repairing and Biotechnology Research Center, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Yunyun ZhuoDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Yanzhu HuDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Zetong ZhangDepartment of Orthopedics, Southwest Hospital, Third Military Medical University, Army Medical University, Chongqing 400038, China.
Jixing YeTissue Repairing and Biotechnology Research Center, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Liehua LiuDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Lei LuoDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Chen ZhaoDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Qiang ZhouDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Pei LiDepartment of Orthopedics, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.
Chongqing Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanical overloading-induced nucleus pulposus (NP) cells senescence plays an important role in the pathogenesis of intervertebral disc degeneration (IVDD). The silent mating type information regulator 2 homolog-1 (SIRT1)-mediated pathway preserves the normal NP cell phenotype and mitochondrial homeostasis under multiple stresses. We aimed to investigate the role of SIRT1 in IVDD by assessing the effects of SIRT1 overexpression on high-magnitude compression-induced senescence in NP cells. High-magnitude compression induced cellular senescence and mitochondrial dysfunction in human NP cells. Moreover, SIRT1 overexpression tended to alleviate NP cell senescence and mitochondrial dysfunction under compressive stress. Given the mitophagy-inducing property of SIRT1, activity of mitophagy was evaluated in NP cells to further demonstrate the underlying mechanism. The results showed that SIRT1-overexpression attenuated senescence and mitochondrial injury in NP cells subjected to high-magnitude compression. However, depletion of PINK1, a key mitophagic regulator, impaired mitophagy and blocked the protective role of SIRT1 against compression induced senescence in NP cells. In summary, these results suggest that SIRT1 plays a protective role in alleviating NP cell senescence and mitochondrial dysfunction under high-magnitude compression, the mechanism of which is associated with the regulation of PINK1-dependent mitophagy. Our findings may provide a potential therapeutic approach for IVDD treatment.

Indexed as

Cellular SenescenceMitophagyAdultBioreactorsCells, CulturedFemaleHumansIntervertebral Disc DegenerationMaleMiddle AgedMitochondriaNucleus PulposusOxidative StressPressureProtein KinasesPTEN-Induced Putative KinaseProtein KinasesPTEN-Induced Putative KinaseSIRT1 protein, humanSirtuin 1compressionmitophagynucleus pulposussenescenceSIRT1

Identifiers

PMID32687063
PMCPMC7485741
OpenAlexW3042669884

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.