Evidence map›Paper›PMID 41692944›Full record

ArticleScience China. Life sciences2026

Hematopoiesis could be improved by correcting aberrant bone marrow macrophages polarization in aplastic anemia patients.

Chen-Yuan Li, Dan-Dan Chen, Xin-Yan Zhang, Shu-Qian Tang, Meng-Zhu Shen, Ya-Ting Yu, Zhi-Wei Zhang, Zheng-Li Xu, Yuan-Yuan Zhang, Jin-Song Jia and 5 more

Abstract read
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In one paragraph

Article in Science China. Life sciences, 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.

  1. 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

15 authors.

Chen-Yuan Li *Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Dan-Dan Chen *Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Xin-Yan ZhangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Shu-Qian TangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Meng-Zhu ShenPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Ya-Ting YuPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Zhi-Wei ZhangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Zheng-Li XuPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Yuan-Yuan ZhangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Jin-Song JiaPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Lan-Ping XuPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Yu WangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Xiao-Hui ZhangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China.
Yuan KongPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China. successky@163.com.
Xiao-Jun HuangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Collaborative Innovation Center of Hematology, Peking University, Beijing, 100044, China. huangxiaojun@bjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune-mediated destruction of hematopoietic stem cells (HSCs) is the most recognized mechanism of aplastic anemia (AA); however, the unfavorable therapeutic effect of immunosuppressive therapy (IST) has shown that the pathogenesis of AA is still unclear. Our previous studies revealed that M1 and M2 macrophages (MΦs) in the bone marrow (BM) microenvironment exert opposite effects on hematopoiesis and that their aberrant polarization is involved in poor hematopoietic reconstitution after transplantation. To determine whether aberrant BM MΦs polarization is involved in the occurrence of AA, we established a classic mouse model of AA and performed a prospective case-control study involving AA patients and age-matched healthy controls (HCs). BM MΦs polarization was analyzed by flow cytometry. RNA-seq, PCR and Western blot were performed to investigate the underlying mechanism involved. To clarify the effect of thrombopoietin receptor agonist (TPO-RA) on BM MΦs polarization and subsequent impact on hematopoiesis and immunity, we established in vitro coculture assays of HSCs/T cells and BM MΦs treated with or without hetrombopag (HET), a novel TPO-RA. We found that in mice with AA, aberrant BM MΦs polarization, characterized by increased M1 MΦs number and decreased M2 MΦs number, accompanied by hematopoietic failure, was observed. Consistently, aberrant BM MΦs polarization, which is related to the downregulation of the PI3K/AKT pathway, was observed in AA patients. HET corrected the aberrant polarization of BM MΦs in AA patients and therefore improved their impaired functions, especially their hematopoiesis-supporting and immune-regulatory abilities, which may be related to the activation of the PI3K/AKT pathway. Although further validation is needed, our data suggest that remodeling BM MΦs polarization may be one of the reasons for the better clinical response to the combination of HET and IST in AA patients.

Indexed as

Anemia, AplasticHematopoiesisMacrophagesAdultAnimalsBone MarrowBone Marrow CellsCase-Control StudiesDisease Models, AnimalFemaleHematopoietic Stem CellsHumansMaleMiceMice, Inbred C57BLProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-aktReceptors, Thrombopoietinaplastic anemiabone marrow microenvironmenthematopoiesismacrophagePI3K/AKT pathway

Identifiers

PMID41692944

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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.