Evidence map›Paper›PMID 38130773›Full record

ArticleJBMR plus2023

P7C3 Ameliorates Bone Loss by Inhibiting Osteoclast Differentiation and Promoting Osteogenesis.

Bo Tian, Jinyu Bai, Lei Sheng, Hao Chen, Wenju Chang, Yue Zhang, Chenlu Yao, Chenmeng Zhou, Xiaoyu Wang, Huajian Shan and 3 more

Open access · goldAbstract read
In one paragraph

Article in JBMR plus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 36% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. NAD metabolism and heart failure: Mechanisms and therapeutic potentials.Journal of molecular and cellular cardiology · 2024
    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

13 authors at 1 institution in 1 country.

Bo TianDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.
Jinyu BaiDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.
Lei ShengDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.
Hao ChenDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.
Wenju ChangDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.
Yue ZhangLaboratory for Biomaterial and ImmunoEngineering, Institute of Functional Nano & SoftMaterials (FUNSOM) Soochow University Suzhou China.
Chenlu YaoLaboratory for Biomaterial and ImmunoEngineering, Institute of Functional Nano & SoftMaterials (FUNSOM) Soochow University Suzhou China.
Chenmeng ZhouLaboratory for Biomaterial and ImmunoEngineering, Institute of Functional Nano & SoftMaterials (FUNSOM) Soochow University Suzhou China.
Xiaoyu WangLaboratory for Biomaterial and ImmunoEngineering, Institute of Functional Nano & SoftMaterials (FUNSOM) Soochow University Suzhou China.
Huajian ShanDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.
Qirong DongDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.
Chao WangLaboratory for Biomaterial and ImmunoEngineering, Institute of Functional Nano & SoftMaterials (FUNSOM) Soochow University Suzhou China.
Xiaozhong ZhouDepartment of Orthopedics The Second Affiliated Hospital of Soochow University Suzhou China.ORCID https://orcid.org/0000-0002-2442-1171
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone homeostasis, the equilibrium between bone resorption and formation, is essential for maintaining healthy bone tissue in adult humans. Disruptions of this process can lead to pathological conditions such as osteoporosis. Dual-targeted agents, capable of inhibiting excessive bone resorption and stimulating bone formation, are being explored as a promising strategy for developing new treatments to address osteoporosis. In this study, we investigated the effects of P7C3 on bone remodeling and its potential therapeutic role in osteoporosis treatment in mice. Specifically, P7C3 can remarkably suppress receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-induced osteoclast differentiation in bone marrow macrophages via the Akt-NF-κB-NFATc1 signaling pathway. Additionally, RNA sequencing (RNAseq) analysis revealed that P7C3 promoted osteoblast differentiation and function through the Wnt/β-catenin signaling pathway, thereby enhancing bone formation. Furthermore, μCT analysis and histological examination of bone tissues from P7C3-treated mice showed attenuation of both Ti-induced bone erosion and ovariectomy (OVX)-induced bone loss. These findings suggest that P7C3 may have a novel function in bone remodeling and may be a promising therapeutic agent for the treatment of osteoporosis. © 2023 The Authors.

Indexed as

BONE HOMEOSTASISOSTEOBLASTOSTEOCLASTOSTEOPOROSISP7C3

Identifiers

PMID38130773
PMCPMC10731119
OpenAlexW4386478400

What Socratic 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 Socratic graph.