Evidence map›Paper›PMID 40077692›Full record

ReviewNutrients2025

Polymethoxyflavones and Bone Metabolism.

Michiko Hirata, Tsukasa Tominari, Chiho Matsumoto, Urara Kasuga, Keisuke Ikeda, Chisato Miyaura, Florian M W Grundler, Masaki Inada

Abstract readReview
In one paragraph

Review in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

8 authors.

Michiko HirataDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.
Tsukasa TominariDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.ORCID 0000-0001-5683-8951
Chiho MatsumotoDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.
Urara KasugaDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.
Keisuke IkedaDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.
Chisato MiyauraDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.
Florian M W GrundlerInada Research Unit, Institute of Global Innovation Research, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.ORCID 0000-0001-8101-0558
Masaki InadaDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei-shi 184-8588, Tokyo, Japan.

Funding

Grant-in-Aid from the Japan Society for the Promotion of Science (JSPS) KAKENHI 22K05490Institute of Global Innovation Research Non
6 · The paper itself

Abstract

Phytochemicals, such as flavonoids, are bioactive compounds produced by plants, including citrus fruits, that exhibit antioxidant effects on mammalian cells and tissues. Polymethoxyflavones (PMFs) are a family of flavonoids found in the pulp and peel of citrus fruits, and have been reported to have potent antioxidant activity implicated in the prevention of human diseases. Several studies have shown that PMFs have a protective effect on bone resorption in mouse models of diseases, including osteoporosis, rheumatoid arthritis, and periodontal disease. PMFs significantly suppressed the differentiation of osteoclasts (bone resorptive cells) through indirect and direct mechanisms. The indirect effect of PMFs is the suppression of inflammatory mediator production, such as prostaglandin E2 (PGE2), and the reduction of osteoclastic inducers, such as the receptor activator of NF-κB ligand (RANKL), in osteoblasts (bone-forming cells). The direct effect of PMF suppresses osteoclast differentiation and function by inhibiting the NF-κB signaling pathway. In silico molecular docking studies indicated that PMFs target the ATP-binding pocket of IKKβ and inhibit the NF-κB signaling pathway. These findings suggest that PMFs protect against bone destruction by interfering with the NF-κB pathway in osteoblasts and osteoclasts. In this review, we summarize the latest findings regarding the effects of PMFs on various bone resorption-related diseases in mouse models.

Indexed as

Bone and BonesBone ResorptionFlavonesAnimalsAntioxidantsCell DifferentiationCitrusHumansMiceNF-kappa BOsteoblastsOsteoclastsSignal TransductionAntioxidantsFlavonesNF-kappa Bbone metabolismbone resorptionosteoblastosteoclastpolymethoxyflavoneprostaglandin E2

Identifiers

PMID40077692
PMCPMC11901578

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.