Evidence map›Paper›PMID 31291980›Full record

ArticleArthritis research & therapy2019

IL-1β receptor antagonist (IL-1Ra) combined with autophagy inducer (TAT-Beclin1) is an effective alternative for attenuating extracellular matrix degradation in rat and human osteoarthritis chondrocytes.

Fen Wang, Jijie Liu, Xiaolei Chen, Xinpeng Zheng, Ning Qu, Bing Zhang, Chun Xia

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06415461 (A Phase 1, Open Label Dose-Ranging Study to Assess the Safety, Tolerability, Preliminary Efficacy, and Dose Effect of CFL001 Cord Blood Product in Patients With Symptomatic Sacroiliac Joint Syndrome), which is not on this map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-weighted citation impact, top 5% 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.

NCT06415461 phase1active not recruitingnot on this mapstarted 2024, after this paper: background citation

A Phase 1, Open Label Dose-Ranging Study to Assess the Safety, Tolerability, Preliminary Efficacy, and Dose Effect of CFL001 Cord Blood Product in Patients With Symptomatic Sacroiliac Joint Syndrome

TypeinterventionalSponsorUniversity of FloridaRan2024 to 2028Enrolled9ConditionsSacroiliac, Backache, Pain, BackArmsPremierMaxCB®-Platinum (CFL001)
3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 55 citations in OpenAlex.

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  8. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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 2 institutions in 1 country.

Fen WangSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Jijie LiuZhongshan Hospital, Xiamen University, Xiamen, 361004, Fujian, China.
Xiaolei ChenZhongshan Hospital, Xiamen University, Xiamen, 361004, Fujian, China.
Xinpeng ZhengZhongshan Hospital, Xiamen University, Xiamen, 361004, Fujian, China.
Ning QuSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Bing ZhangSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China. cristal66@xmu.edu.cn.
Chun XiaZhongshan Hospital, Xiamen University, Xiamen, 361004, Fujian, China. chunxia@xmu.edu.cn.
Zhongshan Hospital of Xiamen University · CNXiamen University · CN

Funding

National Natural Science Foundation of China No. 81572189Xiamen Municipal Bureau of Science and Technology No. 3502Z20154018Xiamen Municipal Bureau of Science and Technology No. 3502Z20159015
6 · The paper itself

Abstract

backgroundAutophagy induction is an effective approach for OA therapy. IL-1β is one of the major inflammatory cytokines linked to OA pathological progression, and its receptor blockade interrupts OA cartilage destruction. The objective of this study was to decipher the link between autophagy and regulatory mechanism of IL-1β and to investigate the effect of IL-1β receptor blockade by IL-1 receptor antagonist (IL-1Ra) combined with or without an autophagy inducer (TAT-Beclin1) on extracellular matrix (ECM) in OA chondrocytes in vitro and in vivo.

methodsIL-1β-treated rat and human OA chondrocytes were cultured in response to IL-1Ra. The expression and distribution of signal molecules regulating ECM synthesis and autophagy were investigated via western blotting, immunoprecipitation, real-time PCR, immunofluorescence, and transmission electron microscope technique. Furthermore, after intra-articular injection of IL-1Ra, TAT-Beclin1, and a combination of both in a rat OA model established by anterior cruciate ligament transection and medial meniscus resection, the morphological changes of cartilage and related signal molecule expression levels were monitored using H.E., Safranin O-Fast green, and immunohistochemistry staining.

resultsReduced autophagy by IL-1β contributed to ECM degradation, and blockade of IL-1β by IL-1Ra restored autophagy and attenuated ECM degradation in rat and human OA chondrocytes, as well as in a rat OA model. Akt/mTOR/ULK1, Akt/mTOR/NF-κB, and LC3B deacetylation were involved in autophagy regulated by IL-1β. Intra-articular injection of IL-1Ra combined with TAT-Beclin1 was more effective than IL-1Ra alone.

conclusionsIL-1Ra restored autophagy and attenuated ECM degradation, with an implication that blocking IL-1β combined with enhancing autophagy might be a potential therapeutic strategy for OA.

Indexed as

AnimalsAnimals, NewbornAntirheumatic AgentsAutophagyCells, CulturedChondrocytesExtracellular MatrixFemaleHumansInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinMaleMiddle AgedOsteoarthritisRats, Sprague-DawleyReceptors, Interleukin-1Antirheumatic AgentsInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinReceptors, Interleukin-1AutophagyECMIL-1RaIL-1βOA chondrocytesRat OA model

Identifiers

PMID31291980
PMCPMC6617669
OpenAlexW2960291519

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.