Evidence map›Paper›PMID 39687521›Full record

ReviewFrontiers in cell and developmental biology2024

The pathogenesis and targeted therapies of intervertebral disc degeneration induced by cartilage endplate inflammation.

Hantao Yang, Xuandu Chen, Jun Chen, Yansong Dong, Yafang Huang, Lei Qin, Jie Tan, Weihong Yi

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 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

20 citing papers in PubMed, 1 synthesis or guideline 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

8 authors.

Hantao Yang *Department of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.
Xuandu Chen *Department of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.
Jun ChenOrthopedic Laboratory, Orthopedic Department and Hubei Sports Medicine Center, Wuhan Fourth Hospital, Wuhan, China.
Yansong DongDepartment of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.
Yafang HuangDepartment of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.
Lei QinDepartment of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.
Jie TanDepartment of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.
Weihong YiDepartment of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intervertebral disc degeneration (IVDD) is the leading cause of low back pain, where degeneration and death of nucleus pulposus cells within the intervertebral disc (IVD) can be obviously revealed. This degeneration can result in an imbalance in the extracellular matrix due to the loss of proteoglycans and water content, which can further lead to catabolic and anabolic dysfunction of the IVD. Recently, the dysfunction of cartilage endplate (CEP) during aging has drawn large attention due to its essential functions in contributing nutrient exchange and maintaining IVD homeostasis. Furthermore, the inflammation and disturbed homeostasis of CEP not only accelerate the degradation of nucleus pulposus extracellular matrix, but also exacerbate IVDD by causing nucleus pulposus cell death through other pathological factors. Here in this review, we summarized the possible pathological factors and the underlying mechanisms of the CEP inflammation-induced IVDD, including exosomes degeneration, CEP calcification, ferroptosis, mechanical changes, and cell senescence. Besides, changes of miRNAs, pain-related neural reflex arc and pathways associated with CEP inflammation-induced IVDD are also reviewed. In addition, new strategies specifically designed for CEP inflammation-induced IVDD are also discussed in the last section. We hope this paper can not only offer some new insights for advancing novel strategies for treating IVDD, but also serve as a valuable reference for researchers in this field.

Indexed as

calcificationcartilage endplateexosomesferroptosisinflammationintervertebral disc degenerationsenescence

Identifiers

PMID39687521
PMCPMC11647014

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.