Evidence map›Paper›PMID 37543947›Full record

ArticleCell reports2023

Autophagy collaborates with apoptosis pathways to control oligodendrocyte number.

Tingxin Zhang, Aksheev Bhambri, Yihe Zhang, Daniela Barbosa, Han-Gyu Bae, Jumin Xue, Sabeen Wazir, Sara B Mulinyawe, Jun Hee Kim, Lu O Sun

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. 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
4.1field-weighted citation impact, top 5% 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, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Tingxin ZhangDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Aksheev BhambriDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Yihe ZhangDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Daniela BarbosaDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Han-Gyu BaeDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center, San Antonio, TX 78229, USA.
Jumin XueDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Sabeen WazirDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Sara B MulinyaweDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Jun Hee KimDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center, San Antonio, TX 78229, USA.
Lu O SunDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Peter O'Donnell Jr. Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: lu.sun@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USThe University of Texas Health Science Center at San Antonio · USSouthwestern Medical Center · USStanford University · US

Funding

Molecular and genetic decoding of neuron-glial interactionsDP2MH129988 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI SUN, LU · 2021 to 2024
$2.6M
Identification of a novel pathway that regulates optic nerve myelination and remyelinationR00EY029330 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI SUN, LU · 2020 to 2022
$884k
TEM for UT Southwestern Electron Microscopy Core FacilityS10OD021685 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI LUBY-PHELPS, KATHERINE J · 2017 to 2017
$398k
NEI NIH HHS R00 EY029330NIH HHS S10 OD021685NIMH NIH HHS DP2 MH129988
6 · The paper itself

Abstract

Oligodendrocytes are the sole myelin-producing cells in the central nervous system. Oligodendrocyte number is tightly controlled across diverse brain regions to match local axon type and number, yet the underlying mechanisms remain unclear. Here, we show that autophagy, an evolutionarily conserved cellular process that promotes cell survival under physiological conditions, elicits premyelinating oligodendrocyte apoptosis during development. Autophagy flux is increased in premyelinating oligodendrocytes, and its genetic blockage causes ectopic oligodendrocyte survival throughout the entire brain. Autophagy functions cell autonomously in the premyelinating oligodendrocyte to trigger cell apoptosis, and it genetically interacts with the TFEB pathway to limit oligodendrocyte number across diverse brain regions. Our results provide in vivo evidence showing that autophagy promotes apoptosis in mammalian cells under physiological conditions and reveal key intrinsic mechanisms governing oligodendrogenesis.

Indexed as

Myelin SheathOligodendrogliaAnimalsApoptosisAutophagyAxonsCell DifferentiationMammalsapoptosisautophagycentral nervous systemCP: Developmental biologyCP: Neurosciencemyelinationoligodendrocyte

Identifiers

PMID37543947
PMCPMC10529879
OpenAlexW4385605619

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.