Evidence map›Paper›PMID 39487546›Full record

ArticleJournal of translational medicine2024

Integrated omics profiling reveals systemic dysregulation and potential biomarkers in the blood of patients with neuromyelitis optica spectrum disorders.

Zuoquan Xie, Qinming Zhou, Jin Hu, Lu He, Huangyu Meng, Xiaoni Liu, Guangqiang Sun, Zhiyu Luo, Yuan Feng, Liang Li and 9 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Acetylcarnitine in cerebrospinal fluid and blood as a protective factor for neuromyelitis optica spectrum disorders: a mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  3. Review
  4. Review
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

19 authors.

Zuoquan Xie *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. zqxie@simm.ac.cn.ORCID 0000-0002-1613-3321
Qinming Zhou *Department of Neurology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
Jin Hu *Department of Neurology, Affiliated Hospital of Jiaxing University, Jiaxing, 314000, China.
Lu HeDepartment of Neurology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
Huangyu MengDepartment of Neurology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
Xiaoni LiuDepartment of Neurology, Huashan Hospital Fudan University and Institute of Neurology, Fudan University, Shanghai, China.
Guangqiang SunShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Zhiyu LuoShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Yuan FengShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Liang LiShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Xingkun ChuShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Chen DuShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Dabing YangShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Xinying YangShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Jing ZhangShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Changrong GeShanghai Green Valley Pharmaceutical Co., Ltd, Shanghai, 201203, China.
Xiang ZhangDepartment of Neurology, Huashan Hospital Fudan University and Institute of Neurology, Fudan University, Shanghai, China. zhangxiang1213@hotmail.com.
Sheng ChenDepartment of Neurology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China. mztcs@163.com.
Meiyu GengState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. mygeng@simm.ac.cn.

Funding

Lingang Laboratory LG202101-01-01National Natural Science Foundation of China 82201558Natural Science Foundation of China for Innovation Research Group 81821005Shandong Laboratory Program SYS202205
6 · The paper itself

Abstract

backgroundNeuromyelitis optica spectrum disorders (NMOSD) are autoimmune conditions that affect the central nervous system. The contribution of peripheral abnormalities to the disease's pathogenesis is not well understood.

methodsTo investigate this, we employed a multi-omics approach analyzing blood samples from 52 NMOSD patients and 46 healthy controls (HC). This included mass cytometry, cytokine arrays, and targeted metabolomics. We then analyzed the peripheral changes of NMOSD, and features related to NMOSD's disease severity. Furthermore, an integrative analysis was conducted to identify the distinguishing characteristics of NMOSD from HC. Additionally, we unveiled the variations in peripheral features among different clinical subgroups within NMOSD. An independent cohort of 40 individuals with NMOSD was utilized to assess the serum levels of fibroblast activation protein alpha (FAP).

resultsOur analysis revealed a distinct peripheral immune and metabolic signature in NMOSD patients. This signature is characterized by an increase in monocytes and a decrease in regulatory T cells, dendritic cells, natural killer cells, and various T cell subsets. Additionally, we found elevated levels of inflammatory cytokines and reduced levels of tissue-repair cytokines. Metabolic changes were also evident, with higher levels of bile acids, lactates, triglycerides, and lower levels of dehydroepiandrosterone sulfate, homoarginine, octadecadienoic acid (FA[18:2]), and sphingolipids. We identified distinctive biomarkers differentiating NMOSD from HC and found blood factors correlating with disease severity. Among these, fibroblast activation protein alpha (FAP) was a notable marker of disease progression.

conclusionsOur comprehensive blood profile analysis offers new insights into NMOSD pathophysiology, revealing significant peripheral immune and metabolic alterations. This work lays the groundwork for future biomarker identification and mechanistic studies in NMOSD, highlighting the potential of FAP as a marker of disease progression.

Indexed as

BiomarkersNeuromyelitis OpticaAdultCase-Control StudiesCytokinesEndopeptidasesFemaleFibroblast Activation Protein AlphaHumansMaleMembrane ProteinsMetabolomicsMiddle AgedBiomarkersCytokinesEndopeptidasesFibroblast Activation Protein AlphaMembrane ProteinsBiomarkerBlood immune cells phenotypingNeuromyelitis optica spectrum disordersPlasma cytokine arrayPlasma metabolomics

Identifiers

PMID39487546
PMCPMC11529322

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.