Evidence map›Paper›PMID 29039595›Full record

ArticleMolecular medicine reports2017

Caveolin‑1 regulates oxidative stress‑induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro.

Lei Ding, Qingmin Zeng, Jingping Wu, Defang Li, Houlei Wang, Wei Lu, Zengxin Jiang, Guoxiong Xu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 22 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 1 institution in 1 country.

Lei DingDepartment of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Qingmin ZengDepartment of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Jingping WuDepartment of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Defang LiDepartment of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Houlei WangDepartment of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Wei LuDepartment of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Zengxin JiangDepartment of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Guoxiong XuCentral Laboratory, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Jinshan Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have indicated that cellular senescence is a critical underlying mechanism of intervertebral disc degeneration. However, the precise mechanism by which cellular senescence accelerates disc degeneration has not been fully elucidated. Caveolin‑1 has recently emerged as an important regulator of cellular senescence. Therefore, the aim of the present study was to investigate whether caveolin‑1 is involved in nucleus pulposus (NP) cellular senescence during oxidative stress. PCR was used to detect caveolin‑1 mRNA expression and protein expression was detected by western blotting. Caveolin‑1 expression at the mRNA and protein levels was markedly increased following treatment with tert‑butyl hydroperoxide, and an increase in premature senescence was observed, as determined by senescence‑associated β‑galactosidase staining and the decline of cellular proliferative ability. In addition, caveolin‑1 gene expression was successfully knocked down by lentivirus‑mediated RNA interference, which exerted a protective effect against the cellular senescence induced by oxidative stress. Notably, p53 and p21 protein expression, though not p16 protein expression, decreased with caveolin‑1 silencing. The results suggested that caveolin‑1 may be involved in NP cellular senescence during oxidative stress in vitro, mainly via the p53/p21 signaling pathway. Thus, caveolin‑1 may represent a novel therapeutic target for the prevention of intervertebral disc degeneration.

Indexed as

Cellular SenescenceOxidative StressSignal TransductionAnimalsCaveolin 1Cyclin-Dependent Kinase Inhibitor p21LentivirusMaleNucleus PulposusRats, Sprague-DawleyRNA InterferenceRNA, Small Interferingtert-ButylhydroperoxideTumor Suppressor Protein p53Caveolin 1Cyclin-Dependent Kinase Inhibitor p21RNA, Small Interferingtert-ButylhydroperoxideTumor Suppressor Protein p53

Identifiers

PMID29039595
PMCPMC5780011
OpenAlexW2761032015

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.