Evidence map›Paper›PMID 41733653›Full record

ReviewCalcified tissue international2026

Macrophage Metabolic Reprogramming-Related Osteoimmunity in Osteoporosis.

Kejia Zhou, Zhenpeng Wang, Mei Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Calcified tissue international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

3 authors.

Kejia ZhouDepartment of Laboratory Medicine, Clinical Laboratory Medicine Research Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Zhenpeng WangDepartment of Laboratory Medicine, Clinical Laboratory Medicine Research Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Mei ZhangDepartment of Laboratory Medicine, Clinical Laboratory Medicine Research Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China. meizhang@wchscu.cn.ORCID http://orcid.org/0000-0002-2076-0563

Funding

Science and Technology Department of Sichuan Province 2024NSFSC0590
6 · The paper itself

Abstract

Osteoporosis is a disease characterized by increased bone turnover and decreased bone mass, closely associated with suppressed osteogenesis, enhanced osteoclastogenesis, and immune-metabolic dysregulation. Studies in osteoimmunology have shown that immune dysregulation can disrupt bone homeostasis through multiple signaling pathways and metabolic interactions between immune cells and bone cells. Macrophages, as key players in osteoimmunity, dynamically alter their metabolism in specific environments, integrating environmental signals to exhibit context-specific functions. Among the primary metabolic phenotypes, classically activated macrophages (M1) mainly promote bone resorption, while alternatively activated macrophages (M2) primarily facilitate osteogenesis. These effects are mainly achieved through inflammatory pathways, macrophage-driven osteoclastogenesis, and efferocytosis. Dysregulation of macrophage metabolic reprogramming in osteoimmunity can lead to diseases such as osteoporosis. The link between metabolic reprogramming and epigenetic modifications is a research hotspot in immune-metabolic diseases, and targeting macrophage metabolic reprogramming has shown potential therapeutic benefits for osteoporosis. This review discusses the impact of macrophage metabolic reprogramming-related osteoimmune pathways on osteoporosis.

Indexed as

MacrophagesOsteoporosisAnimalsHumansMetabolic ReprogrammingOsteoclastsOsteogenesisSignal TransductionMacrophagesMetabolic reprogrammingOsteoimmunityOsteoporosis

Identifiers

PMID41733653

What OpenQuestion holds

Textmetadata
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.