Evidence map›Paper›PMID 41419794›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

Fatty acid binding protein 4 induces osteogenesis and angiogenesis as pathogenesis of metabolic osteoarthritis.

Chaofan Zhang, Yinjun Mao, Yishan Xin, Hongyan Li, Maocan Cai, Yiming Lin, Xuehui Zhang, Ying Huang, Yang Chen, Zida Huang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 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. Review
  2. 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

13 authors.

Chaofan Zhang *Department of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0001-7397-2298
Yinjun Mao *Department of Pharmacy, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0002-4541-9222
Yishan XinDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0009-0003-5013-9916
Hongyan LiDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0001-9300-610X
Maocan CaiDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0009-0008-8711-7135
Yiming LinDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0002-4776-4441
Xuehui ZhangSchool of Health Management, Fujian Medical University, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0002-3991-2379
Ying HuangDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0001-9951-6290
Yang ChenDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0001-7168-7098
Zida HuangDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0002-5204-2005
Xinyu FangDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China.ORCID https://orcid.org/0000-0001-6337-8009
Wenming ZhangDepartment of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China. zhangwm0591@fjmu.edu.cn.ORCID https://orcid.org/0000-0003-1567-7279
Yunzhi LinDepartment of Stomatology, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Rd, Fuzhou, 350005, China. linda_dentist@fjmu.edu.cn.ORCID http://orcid.org/0000-0003-2584-945X

Funding

Joint Funds for the Innovation of Science and Technology, Fujian province 2023Y9061Joint Funds for the Innovation of Science and Technology, Fujian province 2023Y9092Natural Science Foundation of Fujian Province 2023J05131Talent Introduction Scientific Research Project of the First Affiliated Hospital of Fujian Medical University 2022-YJRC3914The First Affiliated Hospital of Fujian Medical University Excellent Talent Program YXRQN-ZCF2023
6 · The paper itself

Abstract

backgroundThe pathogenesis of osteoarthritis (OA) is not yet fully elucidated. FABP4 plays a role in the occurrence of metabolic OA, however, the mechanism remains unclear. The purpose of this study was to further explore the mechanism by which FABP4 mediates the occurrence of metabolic OA.

methodsIn vivo, FABP4 knockout mice (KO) and wild-type littermates (WT) were fed with high-fat diet (HFD) for 3 and 6 months. WT mice were fed with HFD and treated with FABP4 inhibitor BMS309403 (30 mg/kg/d) or vehicle for 6 months. Knee cartilage degenerative changes and subchondral bone changes were assessed. In vitro, FABP4 was used to stimulate mouse bone marrow mesenchymal stem cells (mMSCs) and endothelial progenitor cells (EPCs). Osteogenesis and angiogenesis were assessed.

resultsIn vivo, knocking out of FABP4 and pharmaceutical inhibition of FABP4 significantly alleviated subchondral bone sclerosis and type H vessel formation in mice fed with HFD, and was significantly associated with osteogenesis and angiogenesis. In vitro, FABP4 promotes the differentiation of MSCs into osteoblasts through activation of the PI3K/Akt signaling pathway, and promotes the expression of osteogenesis-related proteins. FABP4 also promotes endothelial cell migration, tube formation, and wound healing through activating the PI3K/Akt pathway.

conclusionsThis study suggests that FABP4 induced subchondral bone osteogenesis and angiogenesis. The PI3K-Akt signaling pathway plays a critical role in both processes. Inhibition of FABP4 may serve as a potential therapeutic approach for metabolic OA.

Indexed as

Fatty Acid-Binding ProteinsNeovascularization, PathologicOsteoarthritisOsteogenesisAngiogenesisAnimalsCell DifferentiationDiet, High-FatDisease Models, AnimalHumansMaleMesenchymal Stem CellsMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene Proteins c-aktFabp4 protein, mouseFatty Acid-Binding ProteinsProto-Oncogene Proteins c-aktAngiogenesisBone remodelingFatty acid binding protein 4 (FABP4)OsteoarthritisSubchondral bone

Identifiers

PMID41419794
PMCPMC12831317

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.