Evidence map›Paper›PMID 40983615›Full record

ArticleNature communications2025

NR3C1-mediated epigenetic regulation suppresses astrocytic immune responses in mice.

Seongwan Park, Hyeonji Park, Youkyeong Gloria Byun, Xiaolin Wei, Junghyun Eom, Jaegeon Joo, Andrew J Lee, Yarui Diao, Won-Suk Chung, Inkyung Jung

Abstract read
In one paragraph

Article in Nature communications, 2025. 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
–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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Astrocyte Functional Heterogeneity in Multiple Sclerosis.Journal of clinical neurology (Seoul, Korea) · 2026
    Review
  9. Article
  10. Article
  11. 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.

Seongwan Park *Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0001-9612-0020
Hyeonji Park *Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Youkyeong Gloria ByunDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0003-4669-0855
Xiaolin WeiDepartment of Cell Biology, Duke University Medical Center, Durham, NC, USA.
Junghyun EomDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Jaegeon JooDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Andrew J LeeDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Yarui DiaoDepartment of Cell Biology, Duke University Medical Center, Durham, NC, USA.ORCID http://orcid.org/0000-0001-5842-4082
Won-Suk ChungDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea. wonsuk.chung@kaist.ac.kr.ORCID http://orcid.org/0000-0003-1060-9007
Inkyung JungDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea. ijung@kaist.ac.kr.ORCID http://orcid.org/0000-0002-5885-2754

Funding

Institute for Basic Science (IBS) IBS-R025-A1National Research Foundation of Korea (NRF) 2021R1A2C3005704National Research Foundation of Korea (NRF) 2022R1A5A1026413National Research Foundation of Korea (NRF) 2023R1A2C3002773National Research Foundation of Korea (NRF) RS-2023-00223069National Research Foundation of Korea (NRF) RS-2023-00262527
6 · The paper itself

Abstract

Astrocytes are critical contributors to brain disorders, yet the mechanisms underlying their selective vulnerability to specific diseases remain poorly understood. Here, we demonstrate that NR3C1 acts as a key regulator of early postnatal astrocyte development, shaping long-term immune responses in mice. Through integrative analyses of gene expression, chromatin accessibility, and long-range chromatin interactions, we identify 55 stage-specific TFs, with NR3C1 uniquely associated with early postnatal maturation. Although mice lacking astrocytic NR3C1 exhibit no detectable developmental abnormalities, these mice display heightened susceptibility to exacerbated immune responses following adult-onset experimental autoimmune encephalomyelitis (EAE). Many of the dysregulated EAE response genes are linked to candidate cis-regulatory elements altered by early NR3C1 loss, driving exacerbated inflammatory responses. Notably, only NR3C1 depletion during early, but not late, astrocyte development induces long-lasting epigenetic reprogramming that primes astrocytic immune responses.

Indexed as

AstrocytesEpigenesis, GeneticReceptors, GlucocorticoidAnimalsCell LineageEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression Regulation, DevelopmentalMaleMiceMice, KnockoutPromoter Regions, GeneticTranscriptomeNR3C1 protein, mouseReceptors, Glucocorticoid

Identifiers

PMID40983615
PMCPMC12454645

What OpenQuestion 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 OpenQuestion graph.