Evidence map›Paper›PMID 42215013›Full record

ReviewReviews in the neurosciences2026

From emergency myelopoiesis to chronic myeloid reprogramming: hematopoietic dysregulation in multiple sclerosis.

Liangyu Gu, Ling Ding, Ziteng Gu, Qizhi Shi, Yunjian Ren, Haihua Zhu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Reviews in the neurosciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Liangyu GuStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, 310000, Hangzhou, China.ORCID https://orcid.org/0009-0004-9333-7370
Ling DingStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, 310000, Hangzhou, China.
Ziteng GuStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, 310000, Hangzhou, China.
Qizhi ShiStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, 310000, Hangzhou, China.
Yunjian RenStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, 310000, Hangzhou, China.
Haihua ZhuStomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Zhejiang Key Laboratory of Oral Biomedical, 310000, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is classically understood through pathogenic T and B cell responses, while increasing evidence indicates that altered myelopoiesis and bone marrow-derived myeloid programs also contribute to disease initiation and progression. This review summarizes the dynamic evolution of hematopoietic dysregulation in MS, proposing a pathological mechanism spanning from transient emergency myelopoiesis to persistent chronic myeloid reprogramming. Driven by sustained inflammatory stress, hematopoietic stem and progenitor cells (HSPCs) undergo epigenetic remodeling to acquire a stable myeloid differentiation bias. Regulatory crosstalk between the inflamed central nervous system (CNS) and the bone marrow may occur through a neuro bone marrow axis involving anatomical fluid drainage, neuroendocrine and circadian regulation, and immune cell feedback loops. This bone marrow-derived reprogramming modulates the downstream effector functions of myeloid cells following their infiltration into the CNS. This framework may refine stage-matched therapeutic thinking in MS by highlighting maladaptive myelopoiesis and immune-homeostatic modulation as potential intervention targets.

Indexed as

chronic myeloid reprogrammingemergency myelopoiesishematopoietic dysregulationmultiple sclerosisneuro bone marrow axis

Identifiers

What Socratic holds

Textmetadata
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.