Evidence map›Paper›PMID 41237782›Full record

ArticleStem cell reports2025

Aging-dependent reduction of KAT7/HBO1 activity impairs imMKCL-based platelet production by promoting immune properties.

Wei-Yin Qiu, Sou Nakamura, Sudip Kumar Paul, Takuya Yamamoto, Naoya Takayama, Naoshi Sugimoto, Si Jing Chen, Koji Eto

Abstract read
In one paragraph

Article in Stem cell reports, 2025. 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

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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

8 authors.

Wei-Yin QiuDepartment of Clinical Application, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
Sou NakamuraDepartment of Clinical Application, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan. Electronic address: sou.nakamura@cira.kyoto-u.ac.jp.
Sudip Kumar PaulDepartment of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Takuya YamamotoDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Institute for the Advanced Study of Human Biology (WPI-ASHBi), Kyoto University, Kyoto, Japan; Medical-risk Avoidance Based on iPS Cells Team, RIKEN Center for Advanced Intelligence Project (AIP), Kyoto, Japan.
Naoya TakayamaDepartment of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Naoshi SugimotoDepartment of Clinical Application, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
Si Jing ChenDepartment of Clinical Application, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Department of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Koji EtoDepartment of Clinical Application, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Department of Regenerative Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan. Electronic address: eto.koji.8a@kyoto-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The master cell bank (MCB) system is essential for regenerative cell therapy. We have developed induced pluripotent stem cell (iPSC)-based immortalized megakaryocyte progenitor cell lines (imMKCLs) as an MCB for iPSC-derived platelet (iPSC-PLT) transfusion. However, imMKCLs exhibit both thrombopoietic and immune-skewed properties, with enhanced immune activity impairing platelet production. The link between immune properties and thrombopoietic efficiency remains unclear. Here, we demonstrate that proliferating imMKCLs in G1 and G2/M interphases contribute to platelet generation, while lysine acetyltransferase 7 (KAT7) suppresses immune-biased dominancy to maintain these interphases. KAT7 inhibition with WM3835 increases G0 cells, mimicking imMKCL aging, and induces cGAS-STING activation, chromatin instability, and the secretion of tumor necrosis factor (TNF)-α, interferon (IFN)-β, and other pro-inflammatory cytokines. Additionally, TNF-α treatment recapitulates the transition to G0 seen with KAT7 loss. These findings identify KAT7 as a key regulator of imMKCL proliferation by preventing immune-skewed properties, highlighting its potential as a quality control marker in iPSC-PLT manufacturing.

Indexed as

AgingBlood PlateletsCellular SenescenceHistone AcetyltransferasesInduced Pluripotent Stem CellsMegakaryocyte Progenitor CellsThrombopoiesisCell LineCell ProliferationHumansHistone Acetyltransferasescell cyclecGAS-STINGimmune megakaryocytelysine acetyltransferase 7

Identifiers

PMID41237782
PMCPMC12744839

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Registered trials

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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.