Evidence map›Paper›PMID 24111943›Full record

ArticleBritish journal of pharmacology2014

Methionine down-regulates TLR4/MyD88/NF-κB signalling in osteoclast precursors to reduce bone loss during osteoporosis.

V Vijayan, M Khandelwal, K Manglani, S Gupta, A Surolia

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
0.6field-weighted citation impact, top 30% 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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

  1. Association between total and animal proteins with risk of fracture: A systematic review and dose-response meta-analysis of cohort studies.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

V VijayanMolecular Sciences Laboratory, National Institute of Immunology, New Delhi, India.
M Khandelwal
K Manglani
S Gupta
A Surolia
National Institute of Immunology · INIndian Institute of Science Bangalore · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeStudies have demonstrated that a moderate intake of amino acids is associated with development of bone health. Methionine, a sulphur-containing essential amino acid, has been largely implicated for improving cartilage formation, however its physiological significance on bone integrity and functionality have not been elucidated. We investigated whether methionine can prevent osteoporotic bone loss. EXPERIMENTAL APPROACH: The anti-resorptive effect of methionine, (250 mg kg(-1) body wt administered in drinking water for 10 weeks), was evaluated in ovariectomized (OVX) rats by monitoring changes in bone turnover, formation of osteoclasts from blood-derived mononuclear cells and changes in the synthesis of pro-osteoclastogenic cytokines. KEY

resultsMethionine improved bone density and significantly decreased the degree of osteoclast development from blood mononuclear cells in OVX rats, as indicated by decreased production of osteoclast markers tartarate resistant acid phosphatase b (TRAP5b) and MIP-1α. siRNA-mediated knockdown of myeloid differentiation primary response 88 [MyD88], a signalling molecule in the toll-like receptor (TLR) signalling cascade, abolished the synthesis of both TRAP5b and MIP-1α in developing osteoclasts. Methionine supplementation disrupted osteoclast development by inhibiting TLR-4/MyD88/NF-κB pathway. CONCLUSIONS AND IMPLICATIONS: TLR-4/MyD88/NF-κB signalling pathway is integral for osteoclast development and this is down-regulated in osteoporotic system on methionine treatment. Methionine treatment could be beneficial for the treatment of postmenopausal osteoporosis.

Indexed as

Acid PhosphataseAdministration, OralAlendronateAnimalsBone DensityBone Density Conservation AgentsBone RemodelingCells, CulturedChemokine CCL3Disease Models, AnimalDose-Response Relationship, DrugDown-RegulationDrug Therapy, CombinationFemaleInflammation MediatorsIsoenzymesAcid PhosphataseAlendronateBone Density Conservation AgentsChemokine CCL3Inflammation MediatorsIsoenzymesMethionineMyd88 protein, ratMyeloid Differentiation Factor 88NF-kappa BTartrate-Resistant Acid PhosphataseTlr4 protein, ratToll-Like Receptor 4alendronatemethionineMyD88osteoclastosteoporosisRANKL

Identifiers

PMID24111943
PMCPMC3874700
OpenAlexW2123139316

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.