Evidence map›Paper›PMID 42135826›Full record

ArticleJournal of translational medicine2026

Targeting mitochondrial calcium homeostasis via novel S100A9 inhibitor B2 as a promising agent against AML.

Chujiao Hu, Junzhao Wan, Dan Ma, Renguang Zhu, Yijuan Wang, Ruiying Li, Ping Wang, Shi Zuo, Lei Tang, Tengxiang Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 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
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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

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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

10 authors.

Chujiao Hu *State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, 561113, China.
Junzhao Wan *State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, 561113, China.
Dan Ma *State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, 561113, China.
Renguang ZhuState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, 561113, China.
Yijuan WangState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, 561113, China.
Ruiying LiState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, 561113, China.
Ping WangDepartment of Hematology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
Shi ZuoPrecision Medicine Research Institute of Guizhou, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China. drzuoshi@gmc.edu.cn.ORCID 0000-0002-8595-5062
Lei TangState Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, 561113, China. tlei1974@gmc.edu.cn.
Tengxiang ChenPrecision Medicine Research Institute of Guizhou, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China. txch@gmc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRelapsed/refractory (R/R) acute myeloid leukemia (AML) remains difficult to treat due to limited actionable targets and frequent drug resistance. Integrated analyses of multiple AML cohorts identified S100A9 as a candidate factor associated with disease aggressiveness and suboptimal therapeutic response in R/R AML.

methodsWe combined genetic perturbation of S100A9 with mitochondrial Ca

resultsS100A9 modulation altered mitochondrial Ca

conclusionsThese findings establish S100A9 as a regulator of mitochondrial Ca

Indexed as

Antineoplastic AgentsCalciumCalgranulin BHomeostasisLeukemia, Myeloid, AcuteMitochondriaAnimalsCell Line, TumorHumansMiceSignal TransductionXenograft Model Antitumor AssaysAntineoplastic AgentsCalciumCalgranulin BAcute myeloid leukemia (AML)Calcium homeostasisInhibitorMitochondriaS100A9

Identifiers

PMID42135826
PMCPMC13439889

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.