Evidence map›Paper›PMID 41816316›Full record

ArticleBioactive materials2026

Artificial mitochondria ameliorates osteoarthritis through restoring cellular energy metabolism homeostasis.

Wenqiang Yan, Yu Chen, Haoda Wu, Zeyuan Gao, Xiaoqing Hu, Yingfang Ao, Chun Mao, Mimi Wan

Abstract read
In one paragraph

Article in Bioactive materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Wenqiang YanDepartment of Sports Medicine, Peking University Third Hospital, Institute of Sports Medicine of Peking University, Beijing, China.
Yu ChenJiangsu Key Laboratory of Biofunctional Materials, Jiangsu Collaborative Innovation Center of Biomedical Functional Materials, National and Local Joint Engineering Research Center of Biomedical Functional Materials, School of Chemistry and Materials Science, Nanjing Normal University, Nanjing, 210023, China.
Haoda WuDepartment of Sports Medicine, Peking University Third Hospital, Institute of Sports Medicine of Peking University, Beijing, China.
Zeyuan GaoDepartment of Sports Medicine, Peking University Third Hospital, Institute of Sports Medicine of Peking University, Beijing, China.
Xiaoqing HuDepartment of Sports Medicine, Peking University Third Hospital, Institute of Sports Medicine of Peking University, Beijing, China.
Yingfang AoDepartment of Sports Medicine, Peking University Third Hospital, Institute of Sports Medicine of Peking University, Beijing, China.
Chun MaoJiangsu Key Laboratory of Biofunctional Materials, Jiangsu Collaborative Innovation Center of Biomedical Functional Materials, National and Local Joint Engineering Research Center of Biomedical Functional Materials, School of Chemistry and Materials Science, Nanjing Normal University, Nanjing, 210023, China.
Mimi WanJiangsu Key Laboratory of Biofunctional Materials, Jiangsu Collaborative Innovation Center of Biomedical Functional Materials, National and Local Joint Engineering Research Center of Biomedical Functional Materials, School of Chemistry and Materials Science, Nanjing Normal University, Nanjing, 210023, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction under pathological or aging conditions disrupts adenosine triphosphate (ATP) synthesis, exacerbating disease progression by skewing energy metabolism toward catabolism. Current strategies to restore metabolic balance remain limited by complexity or inefficiency. Inspired by the phosphocreatine-creatine kinase (CK) system-a mitochondrial-independent energy pathway, we developed chemotactic artificial mitochondria (CAMs) to address this challenge. CAMs consist of crosslinked phosphocreatine monomers (MPCr) and perfluorooctyl acrylate, designed to exploit CK's chemotactic properties for targeted delivery while resisting biofluid interference. CAMs entered degenerated chondrocytes and meniscus fibrochondrocytes via clathrin-mediated endocytosis, escaped lysosomal degradation, scavenged reactive oxygen species, and restored ATP production. Transcriptomic analysis revealed CAMs upregulated chondrogenic markers (

Indexed as

Artificial mitochondriaBioenergetic nanoparticlesDegenerative diseasesEnergy metabolismOsteoarthritis therapy

Identifiers

PMID41816316
PMCPMC12972744

What OpenQuestion holds

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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.