Evidence map›Paper›PMID 37441901›Full record

ArticleBiomaterials2023

Bioactive silica nanoparticles target autophagy, NF-κB, and MAPK pathways to inhibit osteoclastogenesis.

Jamie Arnst, Zhaocheng Jing, Cameron Cohen, Shin-Woo Ha, Manjula Viggeswarapu, George R Beck

Open access · greenAbstract read
In one paragraph

Article in Biomaterials, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.7field-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

17 citing papers in PubMed, 37 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

6 authors at 2 institutions in 2 countries.

Jamie ArnstEmory University, Department of Medicine, Division of Endocrinology, Atlanta, GA, 30322, USA.
Zhaocheng JingEmory University, Department of Medicine, Division of Endocrinology, Atlanta, GA, 30322, USA; The Second Hospital of Shandong University, Department of Orthopedics, Jinan, Shandong, 250033, China.
Cameron CohenEmory University, Department of Medicine, Division of Endocrinology, Atlanta, GA, 30322, USA.
Shin-Woo HaEmory University, Department of Medicine, Division of Endocrinology, Atlanta, GA, 30322, USA.
Manjula ViggeswarapuThe Atlanta Department of Veterans Affairs Medical Center, Decatur, GA, 30033, USA.
George R BeckThe Atlanta Department of Veterans Affairs Medical Center, Decatur, GA, 30033, USA; Emory University, Department of Medicine, Division of Endocrinology, Atlanta, GA, 30322, USA; The Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, 30322, USA. Electronic address: george.beck@emory.edu.
Emory University · USVeterans Health Administration · US

Funding

Targeted nanoparticles for biomedical applicationsR21AR073593 · NIAMS · EMORY UNIVERSITY · PI BECK, GEORGE R. · 2019 to 2020
$378k
Role of phosphate availability in lung cancer invasion and bone metastasisF32CA257436 · NCI · EMORY UNIVERSITY · PI ARNST, JAMIE · 2021 to 2023
$239k
Contribution of Phosphate to Inflammatory Bone LossI01BX001516 · VA · VETERANS HEALTH ADMINISTRATION · PI GEORGE R. BECK · 2019 to 2026
–
Bio-active Nanoparticles and the stimulation of autophagy for improved bone massI01BX002363 · VA · VETERANS HEALTH ADMINISTRATION · PI BECK, GEORGE R. · 2014 to 2017
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BLRD VA I01 BX001516BLRD VA I01 BX002363NCI NIH HHS F32 CA257436NIAMS NIH HHS R21 AR073593
6 · The paper itself

Abstract

Spherical 50 nm silica-based nanoparticles (SiNPs) promote healthy bone homeostasis and maintenance by supporting bone forming osteoblast lineage cells while simultaneously inhibiting the differentiation of bone resorbing osteoclasts. Previous work demonstrated that an intraperitoneal injection of SiNPs in healthy mice - both young and old - increased bone density and quality, suggesting the possibility that SiNPs represent a dual action therapeutic. However, the underlying mechanisms governing the osteoclast response to SiNPs have yet to be fully explored and defined. Therefore, the goals of this study were to investigate the cellular and molecular mechanisms by which SiNPs inhibit osteoclastogenesis. SiNPs strongly inhibited RANKL-induced osteoclast differentiation within the first hours and concomitantly inhibited early transcriptional regulators such as Nfatc1. SiNPs simultaneously stimulated expression of autophagy related genes p62 and LC3β dependent on ERK1/2 signaling pathway. Intriguingly, SiNPs were found to stimulate autophagosome formation while inhibiting the autophagic flux necessary for RANKL-stimulated osteoclast differentiation, resulting in the inhibition of both the canonical and non-canonical NF-κB signaling pathways and stabilizing TRAF3. These results suggest a model in which SiNPs inhibit osteoclastogenesis by inhibiting the autophagic machinery and RANKL-dependent functionality. This mechanism of action defines a novel therapeutic strategy for inhibiting osteoclastogenesis.

Indexed as

Bone ResorptionOsteogenesisAnimalsAutophagyCell DifferentiationMiceNFATC Transcription FactorsNF-kappa BOsteoclastsRANK LigandNFATC Transcription FactorsNF-kappa BRANK LigandAutophagyBone resorptionLC3βNfatc1Osteoporosisp62

Identifiers

PMID37441901
PMCPMC10530178
OpenAlexW4383215599

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.