Evidence map›Paper›PMID 40722393›Full record

ArticleBioengineering (Basel, Switzerland)2025

Pharmacological Intervention with 4-Phenylbutyrate Ameliorates TiAl6V4 Nanoparticles-Induced Inflammatory Osteolysis by Promoting Macrophage Apoptosis.

Guoyin Liu, Haiyang Gong, Tianting Bai, Yahui Fu, Xin Li, Junhao Lu, Jianning Zhao, Jianmin Chen

Abstract read
In one paragraph

Article in Bioengineering (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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.

Guoyin LiuDepartment of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210093, China.ORCID 0000-0001-5570-4564
Haiyang GongDepartment of Rehabilitation, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210093, China.
Tianting BaiDepartment of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210093, China.
Yahui FuMedical School, Nanjing University, Nanjing 210001, China.
Xin LiDepartment of Orthopedics, Central Military Commission Joint Logistics Support Force 904th Hospital, Wuxi 214044, China.
Junhao LuDepartment of Orthopedics, Nanjing Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210022, China.
Jianning ZhaoDepartment of Orthopedics, Nanjing Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210022, China.
Jianmin ChenDepartment of Orthopedics, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210093, China.

Funding

Key Grant Project of Chinese Medicine Education Assciation No. 2024KTM021National Natural Science Foundation of China NSFC. 82102547Natural Science Foundation of Jiangsu Province BK. 20181113Research Project of National Association of Health Industry and Enterprise Management No. ZWB2023001
6 · The paper itself

Abstract

Macrophage apoptosis, along with inflammation in the interface membrane, has been demonstrated to be significant in the pathogenesis and development of particle-induced periprosthetic osteolysis and aseptic loosening. Additionally, the apoptosis of macrophages is considered an indicator of the resolution phase of inflammation and the transition to normal tissue healing. Therefore, targeting macrophages presents a promising strategy for both the prevention and therapeutic management of periprosthetic osteolysis. In this study, we explored the therapeutic potential of chemical chaperone 4-phenylbutyrate (4-PBA) as a pharmacological intervention aimed at modulating macrophage behaviors, particularly focusing on the processes of apoptosis, inflammation, and osteoclastogenesis in a murine model of TiAl6V4 nanoparticle (TiNP)-induced osteolysis. The results derived from in vivo studies conducted on the murine model provide compelling evidence that TiNPs could trigger osteolysis, activate inflammatory cell infiltration, and promote the differentiation of osteoclasts, accompanied by a notable rise in apoptosis at the osteolytic interface periosteum. The severity of TiNP-induced osteolysis, chaotic bone morphology, extensive bone erosion and destruction, occurrence of infiltrating inflammatory cells, and quantity of osteoclasts were attenuated following co-intervention with 4-PBA. Furthermore, the levels of apoptosis, in conjunction with apoptosis-regulated proteins Bcl-2 and Bax, were accentuated following 4-PBA co-intervention, indicating that the TiNP-induced osteolytic interface periosteum environment exhibited a greater propensity for apoptosis due to the pharmacological intervention of 4-PBA. Notably, the use of 4-PBA as a standalone treatment demonstrated comparatively low levels of toxicity and was deemed to be experimentally safe in mice. These findings indicated that 4-PBA may ameliorate the severity of particle-induced osteolysis by inhibiting the inflammatory response and promoting macrophage apoptosis in a manner that may be beneficial for therapeutic strategies. Thus, pharmacological intervention with 4-PBA appears to be a viable option for addressing osteolysis and aseptic loosening resulting from exposure to wear particles, combining efficacy in promoting apoptosis with a favorable safety profile.

Indexed as

4-phenylbutyrateapoptosisaseptic looseninginflammationosteolysiswear particles

Identifiers

PMID40722393
PMCPMC12292459

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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.