Evidence map›Paper›PMID 40873591›Full record

ReviewFrontiers in immunology2025

Oxidative stress and inflammation: roles in osteoporosis.

Jing Luo, Li Li, Wensen Shi, Kangjie Xu, Yucheng Shen, Bin Dai

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 5 pooled it
–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

82 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
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  4. Pharmacological effects ofFrontiers in pharmacology · 2026
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  6. Review
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  10. A microbiota-substrate-metabolite-target network suggests AKT1-associated links between gut microbiota-derived metabolites and osteoporosis.International microbiology : the official journal of the Spanish Society for Microbiology · 2026
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  19. Formononetin attenuates glucocorticoid-induced osteoporosis via multiple osteoimmunological pathways: evidence from zebrafish and network pharmacology.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
    Article
  20. Review

22 more citing papers are in PubMed but not listed here.

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

6 authors.

Jing LuoDepartment of Central Laboratory, Binhai County People's Hospital, Yancheng, China.
Li LiDepartment of Central Laboratory, Binhai County People's Hospital, Yancheng, China.
Wensen ShiDepartment of Central Laboratory, Binhai County People's Hospital, Yancheng, China.
Kangjie XuDepartment of Central Laboratory, Binhai County People's Hospital, Yancheng, China.
Yucheng ShenDepartment of Central Laboratory, Binhai County People's Hospital, Yancheng, China.
Bin DaiDepartment of Central Laboratory, Binhai County People's Hospital, Yancheng, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis (OP) is a prevalent bone disease characterized by reduced bone mineral density (BMD) and compromised microstructure, leading to an increased risk of fractures and disability. With an aging global population, OP has become a significant public health issue, affecting over 200 million people worldwide. OP can be classified into primary (type I and type II) and secondary forms, with estrogen deficiency playing a critical role in postmenopausal OP. The pathophysiology of OP involves a complex interplay of factors, including cellular senescence, oxidative stress, inflammation, and hormonal imbalances. Bone homeostasis, maintained by the balance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation, is regulated by various signaling pathways such as receptor activator of nuclear factor-κB ligand/receptor activator of nuclear factor-κB/osteoprotegerin (RANKL/RANK/OPG), interleukin-1/tumor necrosis factor-α (IL-1/TNF-α), and Notch. Disruption of these pathways, along with oxidative stress and chronic inflammation, leads to bone loss. Estrogen deficiency enhances pro-inflammatory cytokine production, increases osteoclast differentiation, and accelerates bone resorption. Furthermore, cellular senescence and oxidative stress contribute to reduced osteoblast function and increased adipogenesis in bone marrow mesenchymal stem cells (BMSCs). Chronic inflammation and oxidative stress further exacerbate the imbalance in bone remodeling, promoting osteoclast activity and impairing osteogenesis. Understanding the roles of immune dysregulation, oxidative stress, and inflammation in osteoporosis progression is crucial for developing targeted therapeutic strategies. This review discusses the molecular mechanisms underlying inflammation and oxidative stress in OP, highlights current therapeutic approaches, and proposes future research directions aimed at improving the prevention and treatment of osteoporosis.

Indexed as

InflammationOsteoporosisOxidative StressAnimalsBone RemodelingHumansOsteoblastsOsteoclastsSignal Transductioninflammationosteoporosisoxidative stresssignaling pathwaystherapeutic interventions

Identifiers

PMID40873591
PMCPMC12379731

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.