Evidence map›Paper›PMID 42778683›Full record

ArticleCell death and differentiation2026

Ubiquitination-mediated degradation of NLRX1 drives metabolic vulnerability and accelerates intervertebral disc degeneration.

Zhi Du, Di Wu, Hanpeng Xu, Huaizhen Liang, Dingchao Zhu, Shuchang Peng, Bide Tong, Jie Lei, Xingyu Zhou, Hongchuan Wang and 11 more

Abstract read
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In one paragraph

Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

21 authors.

Zhi Du *Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0002-8704-3868
Di Wu *Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hanpeng Xu *Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huaizhen Liang *Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Dingchao ZhuDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Shuchang PengDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0009-0002-5378-7356
Bide TongDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jie LeiDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xingyu ZhouDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hongchuan WangDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yifan DuDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0009-0008-8398-7686
Zixuan OuDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Junyu WeiDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xinyu LiDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Rui ShiDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zhengdong ZhangDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0002-5869-6472
Bingjin WangDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Kun WangDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiaobo FengDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Cao YangDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. caoyangunion@hust.edu.cn.ORCID http://orcid.org/0000-0002-0058-614X
Yu SongDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. songyu1277@hust.edu.cn.ORCID http://orcid.org/0000-0002-0315-2574

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82072505National Natural Science Foundation of China (National Science Foundation of China) 82130072National Natural Science Foundation of China (National Science Foundation of China) 82505633Natural Science Foundation of Hubei Province (Hubei Provincial Natural Science Foundation) 2021CFA007Shenzhen Science and Technology Innovation Commission JCYJ20240813153421028Shenzhen Science and Technology Innovation Commission JCYJ20250604190927038Shenzhen Science and Technology Innovation Commission SGDX20230116093544006
6 · The paper itself

Abstract

Intervertebral disc degeneration (IVDD) is driven in part by senescence of nucleus pulposus (NP) cells, yet the metabolic defects underlying this process remain incompletely defined. Although NLRX1 has been implicated in mitochondrial quality control, the mechanisms governing its stability and its role in OXPHOS regulation during IVDD remain unclear. Here, we show that oxidative phosphorylation (OXPHOS) progressively declines with increasing IVDD severity and that loss of NLRX1 contributes to this defect by disrupting mitochondrial respiration and redox homeostasis in NP cells. Nlrx1

Identifiers

PMID42778683

What Socratic holds

Textmetadata
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.