Evidence map›Paper›PMID 40144792›Full record

ArticleBioactive materials2025

Regulating macrophage glucose metabolism homeostasis via mitochondrial rheostats by short fiber-microsphere scaffolds for bone repair.

Pengzhen Zhuang, Yu Chen, Yu Zhang, Wu Yang, Guilai Zuo, Jessica M Rosenholm, Zhongmin Wang, Juan Wang, Wenguo Cui, Hongbo Zhang

Abstract read
In one paragraph

Article in Bioactive materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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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

10 authors.

Pengzhen ZhuangDepartment of Radiology, Ruijin Hospital Lu Wan Branch, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, PR China.
Yu ChenDepartment of Radiology, Ruijin Hospital Lu Wan Branch, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, PR China.
Yu ZhangDepartment of Radiology, Ruijin Hospital Lu Wan Branch, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, PR China.
Wu YangDepartment of Radiology, Ruijin Hospital Lu Wan Branch, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, PR China.
Guilai ZuoDepartment of Orthopaedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopaedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, P. R. China.
Jessica M RosenholmPharmaceutical Sciences Laboratory, Faculty of Science and Engineering, Åbo Akademi University, Turku, 20520, Finland.
Zhongmin WangDepartment of Radiology, Ruijin Hospital Lu Wan Branch, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, PR China.
Juan WangDepartment of Orthopaedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopaedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, P. R. China.
Wenguo CuiDepartment of Orthopaedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopaedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, P. R. China.
Hongbo ZhangDepartment of Radiology, Ruijin Hospital Lu Wan Branch, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alterations in glucose metabolism flux induced by mitochondrial function changes are crucial for regulating bone immune homeostasis. The restoration of mitochondrial homeostasis, serving as a pivotal rheostat for balancing glucose metabolism in immune cells, can effectively mitigate inflammation and initiate osteogenesis. Herein, an ion-activated mitochondrial rheostat fiber-microsphere polymerization system (FM@CeZnHA) was innovatively constructed. Physical-chemical and molecular biological methods confirmed that CeZnHA, characterized by a rapid degradation rate, releases Ce/Zn ions that restore mitochondrial metabolic homeostasis and M1/M2 balance of macrophages through swift redox reactions. This process reduces the glycolysis level of macrophages by down-regulating the NF-κB p65 signaling pathway, enhances their mitochondrial metabolic dependence, alleviates excessive early inflammatory responses, and promptly initiates osteogenesis. The FM network provided a stable platform for macrophage glycolytic transformation and simulated extracellular matrix microenvironment, continuously restoring mitochondrial homeostasis and accelerating ossification center formation through the release of metal ions from the internal CeZnHA for efficient bone immune cascade reactions. This strategy of bone immunity mediated by the restoration of macrophage mitochondrial metabolic function and glucose metabolic flux homeostasis opens up a new approach to treating bone defects.

Indexed as

Glucose metabolismHydrogel microspheresMitochondrial metabolic homeostasisMitochondrial rheostatShort fibers

Identifiers

PMID40144792
PMCPMC11937614

What OpenQuestion holds

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Registered trials

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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.