Evidence map›Paper›PMID 41455469›Full record

ArticleStem cell reports2026

Hsp70-Bim interaction mediated mitophagy as a potential therapeutic target for CML stem cells.

Ting Song, Yang Song, Hong Zhang, Zhiyuan Hu, Fangkui Yin, Maojun Jiang, Yanxin Zhang, Ziqian Wang, Zhichao Zhang

Abstract read
In one paragraph

Article in Stem cell reports, 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

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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

9 authors.

Ting SongCentral Hospital of Dalian University of Technology, School of Pharmacy, Faculty of Medicine, Dalian University of Technology, Dalian, Liaoning 116024, China. Electronic address: songting@dlut.edu.cn.
Yang SongCentral Hospital of Dalian University of Technology, Dalian University of Technology, Dalian, Liaoning 116024, China.
Hong ZhangCentral Hospital of Dalian University of Technology, School of Pharmacy, Faculty of Medicine, Dalian University of Technology, Dalian, Liaoning 116024, China.
Zhiyuan HuSchool of Life Science and Technology, Dalian University of Technology, Dalian, Liaoning 116024, China.
Fangkui YinCentral Hospital of Dalian University of Technology, School of Chemistry, Dalian University of Technology, Dalian, Liaoning 116024, China.
Maojun JiangCentral Hospital of Dalian University of Technology, School of Pharmacy, Faculty of Medicine, Dalian University of Technology, Dalian, Liaoning 116024, China.
Yanxin ZhangSchool of Life Science and Technology, Dalian University of Technology, Dalian, Liaoning 116024, China.
Ziqian WangCentral Hospital of Dalian University of Technology, School of Pharmacy, Faculty of Medicine, Dalian University of Technology, Dalian, Liaoning 116024, China.
Zhichao ZhangCentral Hospital of Dalian University of Technology, School of Pharmacy, Faculty of Medicine, Dalian University of Technology, Dalian, Liaoning 116024, China. Electronic address: zczhang@dlut.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In chronic myeloid leukemia (CML), disease persistence in patients is maintained by leukemic stem cells (LSCs), which drive tyrosine kinase inhibitor (TKI) resistance. Autophagy has been proposed as a potential therapy to eradicate CML LSCs. Here, using a small-molecule inhibitor of Hsp70 (heat shock protein 70)-Bim (Bcl-2-interacting mediator of cell death) interaction, S1-10, we demonstrate that Hsp70-Bim is a target for CML stemness maintenance. Hsp70-Bim is driven by Bcr-Abl and mediates particularly stronger mitophagy in CML LSCs than differentiated CML cells and HSCs. The more selective mitophagy regulation of Hsp70-Bim than ULK1 (unc-51-like autophagy activating kinase 1) is illustrated. Pharmacological inhibition of Hsp70-Bim blocks mitophagy, leading to the differentiation of CML LSCs, loss of quiescence, and loss of LSC self-renewal potential. In the patient-derived xenograft (PDX) CML models, S1g-10 reduces the number of LSCs by more than 80% after two weeks of injection, without obvious toxicity on normal red blood cells.

Indexed as

Bcl-2-Like Protein 11HSP70 Heat-Shock ProteinsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMitophagyNeoplastic Stem CellsAnimalsCell DifferentiationCell Line, TumorFusion Proteins, bcr-ablHumansMiceProtein BindingXenograft Model Antitumor AssaysBcl-2-Like Protein 11Fusion Proteins, bcr-ablHSP70 Heat-Shock Proteinschronic myeloid leukemiaHsp70-Bimleukemia stem cellsmitophagytyrosine kinase inhibitor

Identifiers

PMID41455469
PMCPMC12925951

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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.