Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.

Hong-Gyun Lee, Joseph M Rone, Joon-Hyuk Lee, Francisco J Quintana

Abstract readReview

In one paragraph

Review in Nature reviews. Immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

1 citing paper in PubMed.

Reduced Arpc1b expression in astrocytes is associated with cytoskeletal remodeling, ALDOA redistribution, glycolysis, and neuroinflammation in a mouse model of bone cancer pain.Translational cancer research · 2026
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

4 authors.

Hong-Gyun Lee *School of Biological Sciences, Seoul National University, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0001-5960-5504

Joseph M Rone *Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Joon-Hyuk Lee *Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-6249-4291

Francisco J QuintanaAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. fquintana@bwh.harvard.edu.ORCID http://orcid.org/0000-0001-8156-0736

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Current therapies for relapsing MS primarily target the peripheral immune system but have consistently failed to address mechanisms underlying disease progression, which are thought to involve CNS-resident glial cells such as astrocytes, microglia and oligodendrocytes. Recent technological advances have revealed the functional heterogeneity of these glial cells, highlighting their crucial roles in inflammation, demyelination, remyelination and neurodegeneration. In this Review, we summarize emerging insights into the diversity, function and regulation of glial cells in MS and inflammation in general, highlight their interactions with immune cells and non-immune cells in the CNS, and discuss potential strategies for their therapeutic modulation.

Identifiers

PMID42236914

DOI10.1038/s41586-022-04432-7

What OpenQuestion holds

Textmetadata

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Registered trials

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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.