Evidence map›Paper›PMID 31518335›Full record

ArticleAging2019

Impact of NF-κB pathway on the apoptosis-inflammation-autophagy crosstalk in human degenerative nucleus pulposus cells.

Weiwei Yi, Yafeng Wen, Fuqiang Tan, Xi Liu, Haiyang Lan, He Ye, Bo Liu

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

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
6.3field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 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

7 authors at 4 institutions in 1 country.

Weiwei YiDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yafeng WenDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Fuqiang TanDepartment of Orthopaedic Surgery, Hechuan District People's Hospital of Chongqing, Chongqing, China.
Xi LiuDepartment of Orthopaedic Surgery, The Affiliated Hospital of Guizhou Medical University, Guizhou, China.
Haiyang LanDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
He YeDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Bo LiuDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNFirst People's Hospital of Chongqing · CNGuiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NF-κB pathway has been reported to play a very important role in the process of intervertebral disc degeneration (IVDD). Our results demonstrated that knockdown of NF-κB with P65-siRNA can significantly decrease cell apoptosis and the expression of pro-inflammation factors TNF-α and IL-1β in LPS-induced nucleus pulposus cells (NPCs). However, the molecular mechanism of NF-κB pathway exerting anti-inflammation and anti-apoptosis function remains unclear. Some researchers reported that inhibiting NF-κB pathway can attenuate the catabolic effect by promoting autophagy during inflammatory conditions in rat nucleus pulposus cells. Therefore, we hypothesized that in human NPCs, inhibiting NF-κB pathway may also promote autophagy. Our results indicated that after knockdown of NF-κB, the autophagy was significantly increased and the expression of p-AKT and p-mTOR protein markedly decreased, but the level of autophagy was inhibited after treatment with AKT activator SC79, suggesting the involvement of AKT/mTOR-mediated autophagy was under autophagy activation. However, both LPS-induced NPCs apoptosis and expression of pro-inflammation factors were further increased by pretreatment with the autophagy inhibitor chloroquine (CQ). These suggested that inhibiting NF-κB pathway can promote autophagy and decrease apoptosis and inflammation response in LPS-induced NPCs. Meanwhile, autophagy triggered by NF-κB inhibition plays a protective role against apoptosis and inflammation.

Indexed as

ApoptosisAutophagyCase-Control StudiesCells, CulturedHumansInflammationIntervertebral Disc DegenerationNF-kappa BNucleus PulposusNF-kappa BapoptosisautophagyinflammationNF-κB pathwaynucleus pulposus cells

Identifiers

PMID31518335
PMCPMC6756901
OpenAlexW2972861106

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.