Evidence map›Paper›PMID 38546949›Full record

ArticleHuman cell2024

Compensatory upregulation of MT2A alleviates neurogenic intermittent claudication through inhibiting activated p38 MAPK-mediated neuronal apoptosis.

Chenggang Wang, Zhanchao Wang, Ying Zi, Xuejian Dan, Jiahui Xu, Jingwei Zhao, Wei Xu, Zhourui Wu, Wei Liu, Bin Ma

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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.

Chenggang Wang *Division of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Zhanchao Wang *Department of Orthopedics, Chongming Hospital Affiliated to Shanghai University of Medicine and Health Sciences, Shanghai, China.
Ying ZiDepartment of Orthopedics, Air Force Hospital of the Northern Theater of Chinese People's Liberation Army (PLA), Shenyang, Liaoning, China.
Xuejian DanDivision of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Jiahui XuDivision of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Jingwei ZhaoDivision of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Wei XuDivision of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Zhourui WuDivision of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Wei LiuDivision of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Bin MaDivision of Spine, Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China. mabin1995@tongji.edu.cn.
Tongji University · CNTongji Hospital · CNChinese People's Liberation Army · CNShanghai University of Medicine and Health Sciences · CN

Funding

the National Natural Science Foundation of China 82071365
6 · The paper itself

Abstract

Neurogenic intermittent claudication (NIC), a classic symptom of lumbar spinal stenosis (LSS), is associated with neuronal apoptosis. To explore the novel therapeutic target of NIC treatment, we constructed the rat model of NIC by cauda equina compression (CEC) method and collected dorsal root ganglion (DRG) tissues, a region responsible for sensory and motor function, for mRNA sequencing. Bioinformatic analysis of mRNA sequencing indicated that upregulated metallothionein 2A (MT2A), an apoptosis-regulating gene belonging to the metallothionein family, might participate in NIC progression. Activated p38 MAPK mediated motor dysfunction following LSS and it was also found in DRG tissues of rats with NIC. Therefore, we supposed that MT2A might affect NIC progression by regulating p38 MAPK pathway. Then the rat model of NIC was used to explore the exact role of MT2A. Rats at day 7 post-CEC exhibited poorer motor function and had two-fold MT2A expression in DRG tissues compared with rats with sham operation. Co-localization analysis showed that MT2A was highly expressed in neurons, but not in microglia or astrocytes. Subsequently, neurons isolated from DRG tissues of rats were exposed to hypoxia condition (3% O

Indexed as

Intermittent Claudicationp38 Mitogen-Activated Protein KinasesAnimalsApoptosisHypoxiaMetallothioneinNeuronsRatsRNA, MessengerUp-RegulationMetallothioneinp38 Mitogen-Activated Protein KinasesRNA, MessengerCell apoptosisMetallothionein 2ANeurogenic intermittent claudicationNeuronp38 MAPK

Identifiers

PMID38546949
OpenAlexW4393268103

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.