Evidence map›Paper›PMID 34494933›Full record

ArticleCell cycle (Georgetown, Tex.)2021

Atorvastatin inhibited TNF-α induced matrix degradation in rat nucleus pulposus cells by suppressing NLRP3 inflammasome activity and inducing autophagy through NF-κB signaling.

Jiancong Chen, Jiansen Yan, Shuangxing Li, Jianxiong Zhu, Jie Zhou, Jun Li, Yangyang Zhang, Zhengqi Huang, Liang Yuan, Kang Xu and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.6field-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

26 citing papers in PubMed, 44 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

12 authors at 4 institutions in 1 country.

Jiancong ChenDepartment of Orthopedics, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jiansen YanGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Shuangxing LiGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Jianxiong ZhuDepartment of Orthopedics, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jie ZhouGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Jun LiGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Yangyang ZhangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Zhengqi HuangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Liang YuanGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Kang XuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Weijian ChenDepartment of Orthopedics, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Wei YeGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen Memorial Hospital · CNSun Yat-sen University · CNGuangzhou Medical University · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intervertebral disc degeneration (IDD) is one of the main causes of lower back pain (LBP). It results from an imbalance between the degradation and synthesis of extracellular matrix (ECM) components in nucleus pulposus (NP) cells. Atorvastatin, an HMG-CoA reductase inhibitor, plays a vital role in many diseases, such as cardiovascular disease and osteoarthritis. However, the effect of atorvastatin on IDD is unclear. Herein, we demonstrated that atorvastatin affects matrix degradation induced by TNF-α and demonstrated the mechanism by which TNF-α modulates matrix metabolism in rat NP cells. Real-time PCR, western blotting and immunofluorescence staining were performed to detect the mRNA and protein expression of related genes. mRFP-GFP-LC3 adenovirus plasmid transfection and transmission electron microscopy (TEM) were used to detect cell autophagy. NLRP3 inhibitor and lentiviral vectors containing shRNA-NLRP3 were used to show the effect of NLRP3 on autophagic flux and the NF-κB signaling pathway. The results revealed that atorvastatin might suppress matrix degradation induced by TNF-α by suppressing NLRP3 inflammasome activity and inducing autophagic flux. Moreover, atorvastatin suppressed NF-κB signaling induced by TNF-α. NF-κB signaling inhibition suppressed NLRP3 inflammasome activity, and NLRP3 inhibition suppressed NF-κB signaling activation induced by TNF-α. NLRP3 inhibition or NLRP3 knockdown induced autophagic flux in the presence of TNF-α. Overall, the present study demonstrated that atorvastatin might suppress matrix degradation induced by TNF-α and further revealed the crosstalk among NLRP3 inflammasome activity, autophagy and NF-κB signaling.

Indexed as

Intervertebral Disc DegenerationNucleus PulposusAnimalsAtorvastatinAutophagyInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinRatsSignal TransductionTumor Necrosis Factor-alphaAtorvastatinInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratTumor Necrosis Factor-alphaatorvastatinautophagyIntervertebral disc degenerationNF-κB signalingNLRP3 inflammasome activity

Identifiers

PMID34494933
PMCPMC8565837
OpenAlexW3197004207

What OpenQuestion holds

Textmetadata
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.