Evidence map›Paper›PMID 42192449›Full record

ArticleJournal of nanobiotechnology2026

Dihydroxyacetone nanoparticles ameliorate osteoarthritis via P21-mediated regulation of chondrocyte repair.

Chao Fang, Zhou Ji, Yankai Pan, Zhi Li, Chenxu Liu, Xinzhe Feng

Abstract read
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In one paragraph

Article in Journal of nanobiotechnology, 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
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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

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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

6 authors.

Chao Fang *Department of Orthopedics, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Zhou Ji *Department of Joint Bone Disease Surgery, Changhai Hospital, Naval Medical University, Shanghai, 200433, China.
Yankai Pan *Department of Joint Bone Disease Surgery, Changhai Hospital, Naval Medical University, Shanghai, 200433, China.
Zhi LiDepartment of Joint Bone Disease Surgery, Changhai Hospital, Naval Medical University, Shanghai, 200433, China.
Chenxu LiuDepartment of Joint Bone Disease Surgery, Changhai Hospital, Naval Medical University, Shanghai, 200433, China.
Xinzhe FengDepartment of Joint Bone Disease Surgery, Changhai Hospital, Naval Medical University, Shanghai, 200433, China. fengxinzheazxc@smmu.edu.cn.

Funding

Doctoral Research Initiation Foundation of the First Affiliated Hospital of the USTC RC2021133National Natural Science Foundation of China 82402766Postdoctoral Research Foundation of China 2023M733424
6 · The paper itself

Abstract

Osteoarthritis (OA) is a disease characterized by progressive cartilage degeneration. P21, as a cell cycle regulator, participates in maintaining cartilage homeostasis. This study aimed to evaluate the therapeutic potential of dihydroxyacetone (DHA) and its hyaluronic acid methacrylate (HAMA)-DHA nanoparticles in improving OA through the P21-mediated PI3K/AKT signaling pathway. Findings from the analyzed human cohorts and animal models revealed significantly reduced P21 expression in OA cartilage, which negatively correlated with disease severity within the examined stages. P21 overexpression enhanced chondrocyte anabolism, alleviated oxidative stress, and suppressed catabolic responses, whereas P21 deficiency exacerbated cartilage degeneration. The combined analysis of RNA sequencing and metabolomics indicated that DHA is a key metabolic node regulating P21. DHA treatment restored P21 levels, alleviated oxidative stress via the P21-mediated PI3K/AKT signaling pathway, promoted expression of anabolic markers (SOX9, COL2, and ACAN), and suppressed catabolic markers (MMP13, ADAMTS-4, and COL10). Compared to free DHA, DHA@HAMA nanoparticles significantly enhanced stability, cellular compatibility, and chondroprotective effects while enabling sustained release. This approach was observed to further promote P21-mediated PI3K/AKT signaling, which corresponded with mitigated cartilage erosion, subchondral bone loss, and OA severity. This study establishes that DHA exerts critical protective effects in OA via the P21-mediated PI3K/AKT signaling pathway. DHA@HAMA nanoparticles alleviate OA progression by more effectively enhancing P21 expression and function, offering a promising new therapeutic strategy for OA treatment.

Indexed as

ChondrocytesCyclin-Dependent Kinase Inhibitor p21DihydroxyacetoneNanoparticlesOsteoarthritisAnimalsHumansHyaluronic AcidMaleMiceOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCyclin-Dependent Kinase Inhibitor p21DihydroxyacetoneHyaluronic AcidPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktChondrocyte repairDihydroxyacetoneHyaluronic acid methacrylateOsteoarthritisP21PI3K/AKT signaling

Identifiers

PMID42192449
PMCPMC13393865

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.