Evidence map›Paper›PMID 42575953›Full record

ArticleLeukemia2026

The FOLR2-IRF2BP2 axis mediates erythropoiesis impairment by excess folic acid in myelodysplastic neoplasms.

Chaoying Yang, Yanpeng Wang, Yuanliang Peng, Zeyuan Wang, Zhiming Guo, Xiaojuan Xiao, Haobo Li, Han Gong, Bin Hu, Li Liu and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 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

17 authors.

Chaoying Yang *Department of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Yanpeng Wang *Department of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Yuanliang Peng *Department of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Zeyuan WangDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Zhiming GuoDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Xiaojuan XiaoDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Haobo LiDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Han GongDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Bin HuDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Li LiuDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Min FuDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Pengfei CaoDepartment of Hematology, Xiangya Hospistal, Central South University, Changsha, Hunan, China.
Xiongbing YangDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China.
Jing LiuDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China. liujing2018@csu.edu.cn.ORCID http://orcid.org/0000-0001-5588-3865
Ling NieDepartment of Hematology, Xiangya Hospistal, Central South University, Changsha, Hunan, China. nielingcsu@outlook.com.ORCID http://orcid.org/0000-0002-7500-0983
Xu HanDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China. hx1989345@163.com.ORCID http://orcid.org/0000-0002-9317-774X
Ji ZhangDepartment of Hematology, The Second Xiangya Hospital, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University; Department of Clinical Laboratory, The Affiliated Nanhua Hospital, University of South China, Changsha, Hunan, China. jizhang@fsyy.usc.edu.cn.ORCID http://orcid.org/0000-0002-6610-9805

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelodysplastic neoplasms (MDS) are a group of heterogeneous clonal hematopoietic disorders with a high risk of progression to acute myeloid leukemia. Despite folic acid being an essential vitamin for human development that can be harmful at high levels, it is still unclear how its excess precisely impacts erythropoiesis in MDS patients. Based on non-targeted metabolomics, we identified significantly elevated folic acid levels in both MDS mice and MDS patients. Functional studies revealed that an excess folic acid diet exacerbated anemia in MDS mice, while restricted folic acid intake alleviated disease phenotypes. Mechanistically, excess folic acid promotes the nuclear translocation of FOLR2, which functions as a transcription factor to bind the promoter of IRF2BP2 and drive its expression. Upregulated IRF2BP2 subsequently represses key erythroid transcription factors GATA1 and KLF1, leading to erythroid differentiation arrest. The folic acid-FOLR2-IRF2BP2 axis is upregulated, and high IRF2BP2 expression correlates with poor prognosis in MDS patients. Our study unveils a novel pathological role of folic acid in promoting MDS progression by disrupting hematopoietic stem/progenitor cells and impairing erythropoiesis, suggesting dietary folic acid restriction and targeting FOLR2-IRF2BP2 axis as potential therapeutic strategies. The FOLR2-IRF2BP2 Axis Mediates Erythropoiesis Impairment by Excess Folic Acid in Myelodysplastic Syndromes. In NUP98-HOXD13 transgenic/MDS mice, folic acid content was significantly increased. Excess folic acid diet exacerbated disease symptoms in MDS mice. Reducing folic acid intake significantly alleviated MDS symptoms. Mechanistically, excess folic acid not only promoted the expansion of hematopoietic stem progenitor cells but also disrupted erythropoiesis involving the FOLR2-IRF2BP2 pathway.

Identifiers

PMID42575953

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.