Evidence map›Paper›PMID 35143418›Full record

ArticleThe Journal of clinical investigation2022

Sec13 promotes oligodendrocyte differentiation and myelin repair through autocrine pleiotrophin signaling.

Zhixiong Liu, Minbiao Yan, Wanying Lei, Rencai Jiang, Wenxiu Dai, Jialin Chen, Chaomeng Wang, Li Li, Mei Wu, Ximing Nian and 12 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Senolytic treatment induces oligodendrocyte dysfunction and demyelination in the corpus callosum.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
  14. Article
  15. Review
  16. Ablation ofLife metabolism · 2023
    Article
  17. 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

22 authors at 3 institutions in 3 countries.

Zhixiong LiuDepartment of Neuroscience, Institute of Neurosurgery, and Department of Neurosurgery, The First Affiliated Hospital, State Key Laboratory of Cellular Stress Biology, School of Medicine.
Minbiao YanDepartment of Neuroscience, Institute of Neurosurgery, and Department of Neurosurgery, The First Affiliated Hospital, State Key Laboratory of Cellular Stress Biology, School of Medicine.
Wanying LeiDepartment of Neuroscience, Institute of Neurosurgery, and Department of Neurosurgery, The First Affiliated Hospital, State Key Laboratory of Cellular Stress Biology, School of Medicine.
Rencai JiangSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Wenxiu DaiSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Jialin ChenSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Chaomeng WangSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Li LiSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Mei WuSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Ximing NianSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Daopeng LiSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Di SunSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Xiaoqi LvSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Chaoying WangSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Changchuan XieSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Luming YaoSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Caiming WuSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Jin HuSchool of Life Sciences, Innovation Center for Cell Signaling Network, and.
Naian XiaoDepartment of Neurology, The First Affiliated Hospital, Xiamen University, Fujian, China.
Wei MoDepartment of Neuroscience, Institute of Neurosurgery, and Department of Neurosurgery, The First Affiliated Hospital, State Key Laboratory of Cellular Stress Biology, School of Medicine.
Zhanxiang WangDepartment of Neuroscience, Institute of Neurosurgery, and Department of Neurosurgery, The First Affiliated Hospital, State Key Laboratory of Cellular Stress Biology, School of Medicine.
Liang ZhangDepartment of Neuroscience, Institute of Neurosurgery, and Department of Neurosurgery, The First Affiliated Hospital, State Key Laboratory of Cellular Stress Biology, School of Medicine.
Toxicologie, Pharmacologie et Signalisation Cellulaire · FRNeurosciences Institute · USFirst Affiliated Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunction of protein trafficking has been intensively associated with neurological diseases, including neurodegeneration, but whether and how protein transport contributes to oligodendrocyte (OL) maturation and myelin repair in white matter injury remains unclear. ER-to-Golgi trafficking of newly synthesized proteins is mediated by coat protein complex II (COPII). Here, we demonstrate that the COPII component Sec13 was essential for OL differentiation and postnatal myelination. Ablation of Sec13 in the OL lineage prevented OPC differentiation and inhibited myelination and remyelination after demyelinating injury in the central nervous system (CNS), while improving protein trafficking by tauroursodeoxycholic acid (TUDCA) or ectopic expression of COPII components accelerated myelination. COPII components were upregulated in OL lineage cells after demyelinating injury. Loss of Sec13 altered the secretome of OLs and inhibited the secretion of pleiotrophin (PTN), which was found to function as an autocrine factor to promote OL differentiation and myelin repair. These data suggest that Sec13-dependent protein transport is essential for OL differentiation and that Sec13-mediated PTN autocrine signaling is required for proper myelination and remyelination.

Indexed as

Demyelinating DiseasesMyelin SheathAutocrine CommunicationCarrier ProteinsCell DifferentiationCytokinesHumansOligodendrogliaCarrier ProteinsCytokinespleiotrophinCell BiologyDemyelinating disordersMultiple sclerosisNeuroscienceProtein traffic

Identifiers

PMID35143418
PMCPMC8970680
OpenAlexW4210968585

What OpenQuestion 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 OpenQuestion graph.