Evidence map›Paper›PMID 26757819›Full record

ArticleThe Journal of biological chemistry2016

Anabolic and Antiresorptive Modulation of Bone Homeostasis by the Epigenetic Modulator Sulforaphane, a Naturally Occurring Isothiocyanate.

Roman Thaler, Antonio Maurizi, Paul Roschger, Ines Sturmlechner, Farzaneh Khani, Silvia Spitzer, Monika Rumpler, Jochen Zwerina, Heidrun Karlic, Amel Dudakovic and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.9field-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.

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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  8. Alternative Medical Therapy.Indian journal of orthopaedics · 2023
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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

15 authors at 4 institutions in 3 countries.

Roman ThalerFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria, Department of Orthopedic Surgery and Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, and.
Antonio MauriziDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100 L'Aquila, Italy.
Paul RoschgerFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria.
Ines SturmlechnerFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria.
Farzaneh KhaniDepartment of Orthopedic Surgery and Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, and.
Silvia SpitzerFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria.
Monika RumplerFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria.
Jochen ZwerinaFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria.
Heidrun KarlicFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria.
Amel DudakovicDepartment of Orthopedic Surgery and Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, and.
Klaus KlaushoferFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria.
Anna TetiDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100 L'Aquila, Italy.
Nadia RucciDepartment of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100 L'Aquila, Italy rucci@univaq.it.
Franz VargaFrom the Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of Social Health Insurance Vienna (WGKK) and Austrian Social Insurance for Occupational Risks (AUVA) Trauma Center Meidling, First Medical Department, Hanusch Hospital, 1140 Vienna, Austria, franz.varga@osteologie.at.
Andre J van WijnenDepartment of Orthopedic Surgery and Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, and vanwijnen.andre@mayo.edu.
Hanusch Hospital · ATLudwig Boltzmann Institute of Osteology · ATMayo Clinic · USUniversity of L'Aquila · IT

Funding

Molecular Control of Bone FormationR01AR049069 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WESTENDORF, JENNIFER J · 2003 to 2021
$5.8M
Austrian Science Fund FWF P 24370NIAMS NIH HHS AR049069NIAMS NIH HHS R01 AR049069
6 · The paper itself

Abstract

Bone degenerative pathologies like osteoporosis may be initiated by age-related shifts in anabolic and catabolic responses that control bone homeostasis. Here we show that sulforaphane (SFN), a naturally occurring isothiocyanate, promotes osteoblast differentiation by epigenetic mechanisms. SFN enhances active DNA demethylation viaTet1andTet2and promotes preosteoblast differentiation by enhancing extracellular matrix mineralization and the expression of osteoblastic markers (Runx2,Col1a1,Bglap2,Sp7,Atf4, andAlpl). SFN decreases the expression of the osteoclast activator receptor activator of nuclear factor-κB ligand (RANKL) in osteocytes and mouse calvarial explants and preferentially induces apoptosis in preosteoclastic cells via up-regulation of theTet1/Fas/Caspase 8 and Caspase 3/7 pathway. These mechanistic effects correlate with higher bone volume (∼20%) in both normal and ovariectomized mice treated with SFN for 5 weeks compared with untreated mice as determined by microcomputed tomography. This effect is due to a higher trabecular number in these mice. Importantly, no shifts in mineral density distribution are observed upon SFN treatment as measured by quantitative backscattered electron imaging. Our data indicate that the food-derived compound SFN epigenetically stimulates osteoblast activity and diminishes osteoclast bone resorption, shifting the balance of bone homeostasis and favoring bone acquisition and/or mitigation of bone resorptionin vivo Thus, SFN is a member of a new class of epigenetic compounds that could be considered for novel strategies to counteract osteoporosis.

Indexed as

Activating Transcription Factor 4AnimalsApoptosisBone Density Conservation AgentsBone ResorptionCaspase 8Cell DifferentiationCollagen Type ICollagen Type I, alpha 1 ChainCore Binding Factor Alpha 1 SubunitDioxygenasesDNA-Binding ProteinsDNA MethylationEpigenesis, GeneticFemaleHumansActivating Transcription Factor 4Atf4 protein, mouseBone Density Conservation AgentsCaspase 8Collagen Type ICollagen Type I, alpha 1 ChainCore Binding Factor Alpha 1 SubunitDioxygenasesDNA-Binding ProteinsIsothiocyanatesProto-Oncogene ProteinsRANK LigandRunx2 protein, mouseSp7 protein, mouseSp7 Transcription FactorsulforaphaneSulfoxidesTET1 protein, mouseTet2 protein, mouseTnfsf11 protein, mouseTranscription Factorsboneepigeneticsosteoblastosteoclastosteoporosis

Identifiers

PMID26757819
PMCPMC4807263
OpenAlexW2238643726

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.