Evidence map›Paper›PMID 39123116›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Dysregulated lipid metabolism and intervertebral disc degeneration: the important role of ox-LDL/LOX-1 in endplate chondrocyte senescence and calcification.

Tan Bing, Xiang Shanlin, Wang Jisheng, Hao Jie, Cao Ruichao, Zhang Zhiwei, Yu Bin, Ma Zhaoxin, Hu Zhenming, Zhou Nian

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
–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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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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

10 authors.

Tan BingDepartment of Spine Surgery, The Third Hospital of Mian Yang, Sichuan Mental Health Center, 621000, Mianyang, People's Republic of China.
Xiang ShanlinDepartment of Orthopedics, Orthopedic Laboratory of Chongqing Medical University, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China.
Wang JishengDepartment of Pharmacy, The Third Hospital of Mian Yang, Sichuan Mental Health Center, 621000, Mianyang, People's Republic of China.
Hao JieDepartment of Orthopedics, Orthopedic Laboratory of Chongqing Medical University, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China.
Cao RuichaoDepartment of Orthopedics, Orthopedic Laboratory of Chongqing Medical University, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China.
Zhang ZhiweiDepartment of Radiology, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China.
Yu BinDepartment of Radiology, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China.
Ma ZhaoxinDepartment of Orthopedics, Orthopedic Laboratory of Chongqing Medical University, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China.
Hu ZhenmingDepartment of Orthopedics, Orthopedic Laboratory of Chongqing Medical University, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China.
Zhou NianDepartment of Orthopedics, Orthopedic Laboratory of Chongqing Medical University, The First Affiliated Hospital of Chongqing Medical University, 400000, Chongqing, People's Republic of China. zhounian_2008@126.com.ORCID 0000-0002-2252-7108

Funding

CQMU Program for Youth Innovation in Future Medicine W0187National Natural Science Foundation of China 82102556
6 · The paper itself

Abstract

backgroundLipid metabolism disorders are associated with degeneration of multiple tissues and organs, but the mechanism of crosstalk between lipid metabolism disorder and intervertebral disc degeneration (IDD) has not been fully elucidated. In this study we aim to investigate the regulatory mechanism of abnormal signal of lipid metabolism disorder on intervertebral disc endplate chondrocyte (EPC) senescence and calcification.

methodsHuman intervertebral disc cartilage endplate tissue, cell model and rat hyperlipemia model were performed in this study. Histology and immunohistochemistry were used to human EPC tissue detection. TMT-labelled quantitative proteomics was used to detect differential proteins, and MRI, micro-CT, safranin green staining and immunofluorescence were performed to observe the morphology and degeneration of rat tail intervertebral discs. Flow cytometry, senescence-associated β-galactosidase staining, alizarin red staining, alkaline phosphatase staining, DCFH-DA fluorescent probe, and western blot were performed to detect the expression of EPC cell senescence, senescence-associated secretory phenotype, calcification-related proteins and the activation of cell senescence-related signaling pathways.

resultsOur study found that the highly expressed oxidized low-density lipoprotein (ox-LDL) and Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) in human degenerative EPC was associated with hyperlipidemia (HLP). TMT-labelled quantitative proteomics revealed enriched pathways such as cell cycle regulation, endochondral bone morphogenesis and inflammation. The rat model revealed that HLP could induce ox-LDL, LOX-1, senescence and calcification markers high expression in EPC. Moreover, we demonstrated that ox-LDL-induced EPCs senescence and calcification were dependent on the LOX-1 receptor, and the ROS/P38-MAPK/NF-κB signaling pathway was implicated in the regulation of senescence induced by ox-LDL/LOX-1 in cell model.

conclusionsSo our study revealed that ox-LDL/LOX-1-induced EPCs senescence and calcification through ROS/P38-MAPK/NF-κB signaling pathway, providing information on understanding the link between lipid metabolism disorders and IDD.

Indexed as

Cellular SenescenceChondrocytesIntervertebral Disc DegenerationLipid MetabolismLipoproteins, LDLScavenger Receptors, Class EAdultAnimalsCalcinosisDisease Models, AnimalFemaleHumansIntervertebral DiscMaleMiddle AgedProteomicsLipoproteins, LDLOLR1 protein, humanoxidized low density lipoproteinScavenger Receptors, Class ECell senescence and calcificationIntervertebral disc degenerationLectin-like oxidized low-density lipoprotein receptor 1Lipid metabolism disordersOxidized low-density lipoprotein

Identifiers

PMID39123116
PMCPMC11311918

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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.