Evidence map›Paper›PMID 38531963›Full record

ArticleExperimental & molecular medicine2024

Involvement of DJ-1 in the pathogenesis of intervertebral disc degeneration via hexokinase 2-mediated mitophagy.

Jialiang Lin, Longjie Wang, Yuhao Wu, Qian Xiang, Yongzhao Zhao, Xuanqi Zheng, Shuai Jiang, Zhuoran Sun, Dongwei Fan, Weishi Li

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.5field-weighted citation impact, top 4% of its field
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

11 citing papers in PubMed, 13 citations in OpenAlex.

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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 at 4 institutions in 1 country.

Jialiang LinDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Longjie WangDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Yuhao WuThe Second School of Medicine, Wenzhou Medical University, Wenzhou, China.
Qian XiangDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Yongzhao ZhaoDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Xuanqi ZhengDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Shuai JiangDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Zhuoran SunDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Dongwei FanDepartment of Orthopedics, Peking University Third Hospital, Beijing, China.
Weishi LiDepartment of Orthopedics, Peking University Third Hospital, Beijing, China. puh3liweishi@163.com.
Ministry of Education of the People's Republic of China · CNPeking University · CNPeking University Third Hospital · CNWenzhou Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172480
6 · The paper itself

Abstract

Intervertebral disc degeneration (IDD) is an important pathological basis for degenerative spinal diseases and is involved in mitophagy dysfunction. However, the molecular mechanisms underlying mitophagy regulation in IDD remain unclear. This study aimed to clarify the role of DJ-1 in regulating mitophagy during IDD pathogenesis. Here, we showed that the mitochondrial localization of DJ-1 in nucleus pulposus cells (NPCs) first increased and then decreased in response to oxidative stress. Subsequently, loss- and gain-of-function experiments revealed that overexpression of DJ-1 in NPCs inhibited oxidative stress-induced mitochondrial dysfunction and mitochondria-dependent apoptosis, whereas knockdown of DJ-1 had the opposite effect. Mechanistically, mitochondrial translocation of DJ-1 promoted the recruitment of hexokinase 2 (HK2) to damaged mitochondria by activating Akt and subsequently Parkin-dependent mitophagy to inhibit oxidative stress-induced apoptosis in NPCs. However, silencing Parkin, reducing mitochondrial recruitment of HK2, or inhibiting Akt activation suppressed DJ-1-mediated mitophagy. Furthermore, overexpression of DJ-1 ameliorated IDD in rats through HK2-mediated mitophagy. Taken together, these findings indicate that DJ-1 promotes HK2-mediated mitophagy under oxidative stress conditions to inhibit mitochondria-dependent apoptosis in NPCs and could be a therapeutic target for IDD.

Indexed as

Intervertebral Disc DegenerationMitophagyProtein Deglycase DJ-1AnimalsApoptosisHexokinaseProto-Oncogene Proteins c-aktRatsUbiquitin-Protein LigasesHexokinaseProtein Deglycase DJ-1Proto-Oncogene Proteins c-aktUbiquitin-Protein Ligases

Identifiers

PMID38531963
PMCPMC10984922
OpenAlexW4393392525

What OpenQuestion holds

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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 OpenQuestion graph.