Evidence map›Paper›PMID 37007148›Full record

ArticleFrontiers in oncology2023

Replication stress increases mitochondrial metabolism and mitophagy in FANCD2 deficient fetal liver hematopoietic stem cells.

Makiko Mochizuki-Kashio, Noriko Otsuki, Kota Fujiki, Sherif Abdelhamd, Peter Kurre, Markus Grompe, Atsushi Iwama, Kayoko Saito, Ayako Nakamura-Ishizu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 28% of its field
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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Wdr5-mediated H3K4 methylation facilitates HSPC development via maintenance of genomic stability in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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 at 5 institutions in 2 countries.

Makiko Mochizuki-KashioDepartment of Mieroscopic and Developmental Anatomy, Tokyo Women's Medical University, Tokyo, Japan.
Noriko OtsukiInstitute of Medical Genetics, Tokyo Women's Medical University, Tokyo, Japan.
Kota FujikiDepartment of Hygiene and Fublic Health, Tokyo Women's Medical University, Tokyo, Japan.
Sherif AbdelhamdDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN, United States.
Peter KurreChildren's Hospital of Philadelphia, Comprehensive Bone Marrow Failure Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Markus GrompePapé Family Pediatric Research Institute, Oregon Stem Cell Center, Oregon Health & Science University, Portland, OR, United States.
Atsushi IwamaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kayoko SaitoInstitute of Medical Genetics, Tokyo Women's Medical University, Tokyo, Japan.
Ayako Nakamura-IshizuDepartment of Mieroscopic and Developmental Anatomy, Tokyo Women's Medical University, Tokyo, Japan.
Tokyo Women's Medical University · JPChildren's Hospital of Philadelphia · USOregon Health & Science University · USSt. Jude Children's Research Hospital · USThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fanconi Anemia (FA) is an inherited bone marrow (BM) failure disorder commonly diagnosed during school age. However, in murine models, disrupted function of FA genes leads to a much earlier decline in fetal liver hematopoietic stem cell (FL HSC) number that is associated with increased replication stress (RS). Recent reports have shown mitochondrial metabolism and clearance are essential for long-term BM HSC function. Intriguingly, impaired mitophagy has been reported in FA cells. We hypothesized that RS in FL HSC impacts mitochondrial metabolism to investigate fetal FA pathophysiology. Results show that experimentally induced RS in adult murine BM HSCs evoked a significant increase in mitochondrial metabolism and mitophagy. Reflecting the physiological RS during development in FA, increase mitochondria metabolism and mitophagy were observed in FANCD2-deficient FL HSCs, whereas BM HSCs from adult FANCD2-deficient mice exhibited a significant decrease in mitophagy. These data suggest that RS activates mitochondrial metabolism and mitophagy in HSC.

Indexed as

FANCD2fetal liverHematopoietic stem cellmitochondria metabolismmitophagyreplication stress

Identifiers

PMID37007148
PMCPMC10061350
OpenAlexW4323364212

What Socratic holds

Textmetadata
LicenceCC BY
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.