Evidence map›Paper›PMID 34085175›Full record

ArticleInflammopharmacology2021

Exogenous stromal cell-derived factor-1 (SDF-1) suppresses the NLRP3 inflammasome and inhibits pyroptosis in synoviocytes from osteoarthritic joints via activation of the AMPK signaling pathway.

Shuya Wang, Ali Mobasheri, Yue Zhang, Yanli Wang, Tianqi Dai, Zhiyi Zhang

Open access · hybridAbstract read
In one paragraph

Article in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 34 citations in OpenAlex.

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  14. The Anti-Inflammatory Effect of SDF-1 Derived Peptide onPathogens (Basel, Switzerland) · 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

6 authors at 2 institutions in 4 countries.

Shuya WangDepartment of Rheumatology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng St, Harbin, 150001, China.ORCID http://orcid.org/0000-0002-1031-8907
Ali MobasheriDepartment of Joint Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, Guangdong, China. ali.mobasheri@oulu.fi.ORCID http://orcid.org/0000-0001-6261-1286
Yue ZhangDepartment of Rheumatology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng St, Harbin, 150001, China.
Yanli WangDepartment of Rheumatology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng St, Harbin, 150001, China.
Tianqi DaiDepartment of Rheumatology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng St, Harbin, 150001, China.
Zhiyi ZhangDepartment of Rheumatology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng St, Harbin, 150001, China. zhangzhiyi2014@163.com.
Harbin Medical University · CNSun Yat-sen University · CN

Funding

Harbin Medical University HYD2020YQ0008Lietuvos Mokslo Taryba (LT) DOTSUT-215National Natural Science Foundation of China NSFC81771748National Natural Science Foundation of China NSFC 81771749
6 · The paper itself

Abstract

objectiveNLRP3 inflammasome may play a key role in OA pathogenesis. Stromal cell-derived factor-1 (SDF-1) is a homeostatic CXC chemokine. Since the role of SDF-1 in OA has not been explored, this study aimed to examine the effect of SDF-1 on NLRP3 inflammasome and pyroptosis in synoviocytes from OA joints. MATERIALS AND

methodsHuman synovium was obtained from OA patients for isolation of primary synoviocytes and a murine model of collagenase-induced OA was established for testing intra-articular injections of SDF-1. Immunoblotting assays were used to examine the effects and underlying mechanism of action of SDF-1 on NLRP3 inflammasome and synoviocyte pyroptosis in synoviocytes. Inhibitors of AMPK and PI3K-mTOR were utilized to investigate the key signaling pathways involved in SDF-1-mediated OA inflammasome formation and pyroptosis.

resultsSynoviocytes from OA joints exhibited significantly higher expression of NLRP3 inflammasome and biomarkers of synoviocyte pyroptosis relative to healthy individuals. This was confirmed in the collagenase-induced OA model, where OA synoviocytes had a significantly lower SDF-1 expression than healthy ones. SDF-1 treatment in synoviocytes of OA patients and collagenase-induced OA led to significant downregulation in the expression of NLRP3 inflammasome and synoviocyte pyroptosis biomarkers. Inhibition of the AMPK signaling pathway significantly suppressed the inhibitory effect of SDF-1 on NLRP3 inflammasome expression of OA synoviocytes. However, blocking the SDF-1-activated PI3K-mTOR signaling pathway could still suppress the expression of NLRP3 inflammasome and synoviocyte pyroptosis biomarkers.

conclusionsSDF-1 ameliorates NLRP3 inflammasome and pyroptosis in OA synoviocytes through activation of the AMPK signaling pathway. Therefore, SDF-1 may be a novel therapeutic target for OA.

Indexed as

AMP-Activated Protein KinasesAnimalsCells, CulturedChemokine CXCL12CollagenasesHumansMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinOsteoarthritisPyroptosisSignal TransductionSynoviocytesAMP-Activated Protein KinasesChemokine CXCL12CollagenasesCXCL12 protein, humanNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseLow-grade inflammationNLRP3 inflammasomeOsteoarthritis (OA)PyroptosisStromal cell-derived factor-1SynoviocyteSynovitis

Identifiers

PMID34085175
PMCPMC8233244
OpenAlexW3138464163

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Registered trials

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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.