ArticleVeterinary research2025
Echinococcus granulosus promotes MAPK pathway-mediated osteoclast differentiation by inhibiting Nrf2 in osseous echinococcosis.
Article in Veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Cynarin as a potent anti‑osteolytic agent: Targeting MAPK and Nrf2‑Keap1 pathways for osteoclast inhibition and bone protection.International journal of molecular medicine · 2025Article
- Ferroptosis and bone metabolic diseases: the dual regulatory role of the Nrf2/HO-1 signaling axis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Osseous echinococcosis causes severe "osteolytic" changes in the bone tissue of Echinococcus granulosus (E. granulosus) infection sites by promoting the over-differentiation of osteoclasts at the site. Nrf2 is a key regulator of osteoclast differentiation and formation, and this study investigated the regulatory mechanism by which Nrf2 promotes osteoclast differentiation after E. granulosus infection. In vitro, our study revealed that PSC intervention suppressed the expression levels of intracellular Nrf2 and its downstream effector, heme oxygenase-1 (HO-1), while increasing the content of intracellular reactive oxygen species (ROS), thereby promoting osteoclast differentiation. Next, we treated bone marrow mononuclear cells (BMMCs) with protoscoleces (PSC) and found that Nrf2 knockdown significantly promoted osteoclast formation, whereas Nrf2 activation had the opposite effect. We also verified that phosphorylation of the MAPK pathway was promoted after PSC intervention. In vivo, we established an osseous CE model and reported that Nrf2 knockout mice presented more pronounced bone destruction and more active osteoclast differentiation in infected bone tissue. In this study, we demonstrated that Nrf2 plays an important regulatory role in echinococcosis of the bone caused by E. granulosus infection both in vitro and in vivo. E. granulosus infection inhibits the expression of Nrf2 in cells, which leads to increased osteoclast differentiation and active bone resorption. This study provides not only a direction for more precise mechanistic research but also a new molecular target for the drug treatment of osseous echinococcosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.