Evidence map›Paper›PMID 40090836›Full record

ArticleCell proliferation2025

Targeting FABP4 to Inhibit AGEs-RAGE/NF-κB Signalling Effectively Ameliorates Nucleus Pulposus Dysfunction and Angiogenesis in Obesity-Related Intervertebral Disc Degeneration.

Lin Han, Fudong Li, Huiqiao Wu, Weiheng Wang, Peiwen Chen, Weicheng Xia, Yang Liu, Kaiqiang Sun, Wenbo Lin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 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

9 authors.

Lin HanDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Fudong LiDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0002-3407-0715
Huiqiao WuDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Weiheng WangDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Peiwen ChenDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Weicheng XiaDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Yang LiuDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Kaiqiang SunDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0002-0272-8383
Wenbo LinDepartment of Orthopedic Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.

Funding

Naval Medical University Talent Launch ProgrammeScience and Technology Innovation Action Plan from The Science and Technology Commission of Shanghai Municipality 23Y11903100Shanghai Pujiang Program 21PJD070
6 · The paper itself

Abstract

Intervertebral disc degeneration (IVDD) is a primary contributor to low back pain, posing significant social and economic burdens. Increasing evidence shows that obesity contributes to IVDD, yet the underlying mechanisms remain elusive. Here, we firstly revealed a causal correlation between obesity and IVDD via a two-sample mendelian randomization analysis and identified fatty acid-binding protein 4 (FABP4) as the potential regulator to associate IVDD and obesity. Elevated FABP4 expression promoted extracellular matrix (ECM) disequilibrium and angiogenesis to exacerbate IVDD progression. Genetically knocking out or pharmacologically inhibiting FABP4 in high-fat diet-induced mice alleviated IVDD. Mechanistically, obesity activated the mammalian target of rapamycin complex 1 (mTORC1), which upregulated FABP4 expression, leading to the accumulation of advanced glycation end-products (AGEs) in intervertebral disc tissue. AGEs further activated the NF-κB signalling pathway, exacerbating ECM degradation and neovascularization. Conversely, rapamycin-mediated inhibition of mTORC1 suppressed FABP4 expression in nucleus pulposus cells (NPCs), alleviating IVDD in vivo. Collectively, our findings reveal a critical role of the obesity-induced mTORC1-FABP4 axis in ECM degradation and angiogenesis during IVDD progression. Targeting FABP4 may represent a promising therapeutic strategy for IVDD in obese individuals.

Indexed as

Fatty Acid-Binding ProteinsGlycation End Products, AdvancedIntervertebral Disc DegenerationNeovascularization, PathologicNF-kappa BNucleus PulposusObesityAngiogenesisAnimalsDiet, High-FatExtracellular MatrixHumansMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLFABP4 protein, humanFabp4 protein, mouseFatty Acid-Binding ProteinsGlycation End Products, AdvancedMechanistic Target of Rapamycin Complex 1NF-kappa BangiogenesisECM homeostasisFABP4intervertebral disc degenerationmendelian randomizationobesitysignal pathwaytherapeutic target

Identifiers

PMID40090836
PMCPMC12414640

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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.