Evidence map›Paper›PMID 29242539›Full record

ArticleNature immunology2018

Atad3a suppresses Pink1-dependent mitophagy to maintain homeostasis of hematopoietic progenitor cells.

Guoxiang Jin, Chuan Xu, Xian Zhang, Jie Long, Abdol Hossein Rezaeian, Chunfang Liu, Mark E Furth, Steven Kridel, Boris Pasche, Xiu-Wu Bian and 1 more

Abstract read
In one paragraph

Article in Nature immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing 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

98 citing papers in PubMed.

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  13. Mitochondrial ROS triggers mitophagy through activating the DNA damage response signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Article
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38 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Guoxiang JinInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Chuan XuInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xian ZhangDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Jie LongDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Abdol Hossein RezaeianDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Chunfang LiuDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Mark E FurthWake Forest Innovations, Wake Forest Baptist Medical Center, Winston-Salem, NC, USA.
Steven KridelDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Boris PascheDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Xiu-Wu BianInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China. bianxiuwu@263.net.ORCID http://orcid.org/0000-0003-4383-0197
Hui-Kuan LinDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC, USA. hulin@wakehealth.edu.ORCID http://orcid.org/0000-0002-3501-2410

Funding

Identification of a new strategy for cancer therapyR01CA193813 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LIN, HUI-KUAN · 2015 to 2019
$1.8M
Novel posttranslational modification in LKB1 activation and cancer developmentR01CA182424 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LIN, HUI-KUAN · 2014 to 2018
$1.6M
NCI NIH HHS R01 CA182424NCI NIH HHS R01 CA193813
6 · The paper itself

Abstract

Although deletion of certain autophagy-related genes has been associated with defects in hematopoiesis, it remains unclear whether hyperactivated mitophagy affects the maintenance and differentiation of hematopoietic stem cells (HSCs) and committed progenitor cells. Here we report that targeted deletion of the gene encoding the AAA+-ATPase Atad3a hyperactivated mitophagy in mouse hematopoietic cells. Affected mice showed reduced survival, severely decreased bone-marrow cellularity, erythroid anemia and B cell lymphopenia. Those phenotypes were associated with skewed differentiation of stem and progenitor cells and an enlarged HSC pool. Mechanistically, Atad3a interacted with the mitochondrial channel components Tom40 and Tim23 and served as a bridging factor to facilitate appropriate transportation and processing of the mitophagy protein Pink1. Loss of Atad3a caused accumulation of Pink1 and activated mitophagy. Notably, deletion of Pink1 in Atad3a-deficient mice significantly 'rescued' the mitophagy defect, which resulted in restoration of the progenitor and HSC pools. Our data indicate that Atad3a suppresses Pink1-dependent mitophagy and thereby serves a key role in hematopoietic homeostasis.

Indexed as

HomeostasisMitophagyAnimalsApoptosisATPases Associated with Diverse Cellular ActivitiesCell DifferentiationCell ProliferationHEK293 CellsHematopoietic Stem CellsHumansMembrane ProteinsMembrane Transport ProteinsMice, KnockoutMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsAtad3a protein, mouseATPases Associated with Diverse Cellular ActivitiesMembrane ProteinsMembrane Transport ProteinsMitochondrial Membrane Transport Proteinsmitochondrial outer membrane protein 35-kDa, mouseMitochondrial Precursor Protein Import Complex ProteinsMitochondrial ProteinsProtein KinasesPTEN-Induced Putative KinaseTimm23 protein, mouse

Identifiers

PMID29242539
PMCPMC5905408

What OpenQuestion holds

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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.