Evidence map›Paper›PMID 39653824›Full record

ArticleNature cardiovascular research2024

Clonal hematopoiesis-related mutant ASXL1 promotes atherosclerosis in mice via dysregulated innate immunity.

Naru Sato, Susumu Goyama, Yu-Hsuan Chang, Masashi Miyawaki, Takeshi Fujino, Shuhei Koide, Tamami Denda, Xiaoxiao Liu, Koji Ueda, Keita Yamamoto and 16 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Arteriosclerosis, thrombosis, and vascular biology · 2026
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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

26 authors.

Naru SatoDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-0452-3194
Susumu GoyamaDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-9339-1826
Yu-Hsuan ChangDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Masashi MiyawakiMolecular Pharmacology of Malignant Diseases, Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-Ku, Japan.
Takeshi FujinoDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Shuhei KoideDivision of Stem Cell and Molecular Medicine, Centre for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Tamami DendaDepartment of Pathology, The Institute of Medical Science Research Hospital, University of Tokyo, Tokyo, Japan.
Xiaoxiao LiuDivision of Molecular Oncology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-0023-4013
Koji UedaProject for Personalized Cancer Medicine, Cancer Precision Medicine Centre, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID http://orcid.org/0000-0001-9066-4959
Keita YamamotoDivision of Molecular Oncology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, University of Tokyo, Tokyo, Japan.
Shuhei AsadaThe Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6116-7996
Reina TakedaDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4233-8806
Taishi YonezawaDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Yosuke TanakaDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8538-0916
Hiroaki HondaThe Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4617-9670
Yasunori OtaDepartment of Pathology, The Institute of Medical Science Research Hospital, University of Tokyo, Tokyo, Japan.
Takuma ShibataDepartment of Microbiology and Immunology, Division of Infectious Genetics, University of Tokyo, Tokyo, Japan.
Motohiro SekiyaDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.ORCID http://orcid.org/0000-0002-5170-9699
Tomoya IsobeDepartment of Hematology, Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-3487-3307
Chrystelle LamagnaRigel Pharmaceuticals, Inc., South San Francisco, CA, USA.
Esteban MasudaRigel Pharmaceuticals, Inc., South San Francisco, CA, USA.
Atsushi IwamaDivision of Stem Cell and Molecular Medicine, Centre for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-9410-8992
Hitoshi ShimanoDepartment of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Jun-Ichiro InoueResearch Platform Office, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6389-7036
Kensuke MiyakeDepartment of Microbiology and Immunology, Division of Infectious Genetics, University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6629-226X
Toshio KitamuraDivision of Cellular Therapy, The Institute of Medical Science, University of Tokyo, Tokyo, Japan. kitamura@ims.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0001-7855-1767

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Certain somatic mutations provide a fitness advantage to hematopoietic stem cells and lead to clonal expansion of mutant blood cells, known as clonal hematopoiesis (CH). Among the most common CH mutations, ASXL1 mutations pose the highest risk for cardiovascular diseases (CVDs), yet the mechanisms by which they contribute to CVDs are unclear. Here we show that hematopoietic cells harboring C-terminally truncated ASXL1 mutant (ASXL1-MT) accelerate the development of atherosclerosis in Ldlr

Indexed as

AtherosclerosisClonal HematopoiesisDisease Models, AnimalImmunity, InnateInterleukin-1 Receptor-Associated KinasesMutationRepressor ProteinsSignal TransductionAnimalsAortic DiseasesHumansMacrophagesMaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceAsxl1 protein, mouseInterleukin-1 Receptor-Associated KinasesIrak1 protein, mouseMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BRepressor Proteins

Identifiers

PMID39653824

What OpenQuestion 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 OpenQuestion graph.