Evidence map›Paper›PMID 39392081›Full record

ArticleJournal of cellular and molecular medicine2024

LTF ameliorates cartilage endplate degeneration by suppressing calcification, senescence and matrix degradation through the JAK2/STAT3 pathway.

Tao Li, Yuchi Liu, Jian Cao, Chongzhi Pan, Rui Ding, Jiangminghao Zhao, Jiahao Liu, Dingwen He, Jingyu Jia, Xigao Cheng

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
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  4. Review
  5. Review
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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.

Tao LiDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0000-0002-0675-5952
Yuchi LiuDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0009-0003-7524-2629
Jian CaoDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Chongzhi PanDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Rui DingDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Jiangminghao ZhaoDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Jiahao LiuDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Dingwen HeDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Jingyu JiaDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0000-0001-7128-2621
Xigao ChengDepartment of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, China.ORCID 0000-0002-6105-1499

Funding

Interdisciplinary Innovation Fund of Natural Science, NanChang UniversityNational Natural Science Foundation of China 82060403Thousand Talents Program of Jiangxi Province JXSQ2019201026
6 · The paper itself

Abstract

Intervertebral disc degeneration (IDD)-induced cervical and lumbar herniations are debilitating diseases. The function of intervertebral disc (IVD) mainly depends on the cartilage endplate (CEP), which provides support and waste removal. Therefore, IDD stems from the degeneration of CEP. Our study shows that the expression of lactotransferrin (LTF), an iron-binding protein, is significantly decreased in degenerated human and rat CEP tissues. In addition, we found that LTF knockdown promoted calcification, senescence, and extracellular matrix (ECM) degradation in human endplate chondrocytes. Furthermore, the in vivo experiment results confirmed that the JAK2/STAT3 pathway inhibitor AG490 significantly reversed these effects. In addition to investigating the role and mechanism of LTF in CEP degeneration, this study provides a theoretical basis and experimental evidence to improve IDD treatment.

Indexed as

ChondrocytesExtracellular MatrixIntervertebral Disc DegenerationJanus Kinase 2Signal TransductionSTAT3 Transcription FactorAdultAnimalsCalcinosisCartilageCellular SenescenceFemaleHumansMaleMiddle AgedRatsJanus Kinase 2STAT3 Transcription Factorcalcificationcartilage endplate degenerationextracellular matrix degradationJAK2/STAT3 pathwaylactotransferrinsenescence

Identifiers

PMID39392081
PMCPMC11467740

What OpenQuestion holds

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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.