ArticleCalcified tissue international2025
Osteocyte Neuropeptide Y Aggravates Bone Loss in OVX Mice by Inhibiting Preosteoclast Proliferation and PDGF-BB-Induced Type H Vessel Formation Through PI3K/Akt Signaling Pathway.
Article in Calcified tissue international, 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.
- Osteocyte-vascular Interactions in Bone Physiology and Pathology.Current osteoporosis reports · 2026Review
- Neuropeptide Y in cancer metastasis and chemoresistance.Neuropeptides · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Type H vessels are sensitive markers of bone mass. Platelet-derived growth factor-BB (PDGF-BB) secreted by preosteoclast was linked with type H vessel generation. Osteocytes (OCY) have been reported to modulate bone metabolism through neuronal induction and active molecules. This study aimed to characterize effect of osteocyte-derived neuropeptide Y (NPY) on ovariectomy (OVX)-induced bone loss in mice and explore the underlying mechanism. Monocytes/macrophages (Mo) were isolated and induced into preosteoclast. Small interfering RNAs were used to knockdown NPY expression in OCY. The culture medium was harvested. Preosteoclast proliferation and PDGF-BB expression were measured by CCK8 analysis and ELISA respectively. Angiogenesis-related experiments were conducted to evaluate the effects of NPY and PDGF-BB on angiogenesis. Western blotting clarified PI3K/Akt pathway involvement in NPY-mediated angiogenesis. In vivo, OVX mice received cultured medium from OCY with NPY knockdown, NPY or vehicle through bone marrow cavity injection. After 2 months, bone samples were collected for µCT and immunofluorescent analysis. Serum OCN, PDGF-BB and VEGF concentrations were assessed by ELISA. It was found that osteocyte-derived NPY inhibits preosteoclast proliferation and PDGF-BB secretion. Culture medium from NPY-stimulated preosteoclasts suppressed migration and tube formation of human microvascular endothelial cells and this effect was reversed following PDGF-BB treatment. NPY negatively regulates preosteoclast PDGF-BB-induced angiogenesis through PI3K/Akt signaling. Importantly, osteocyte NPY exerted detrimental effects on type H vessel formation and aggravated bone loss in OVX mice. Our study identifies a new mechanism by which osteocyte-derived NPY accelerates OVX-induced bone mass loss via inhibiting PDGF-BB secretion and type H vessel formation.
Indexed as
Identifiers
41186709What Socratic 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 Socratic graph.