Evidence map›Paper›PMID 40134942›Full record

ArticlemicroPublication biology2025

Potential for micronuclear turnover through autophagy secretion pathway.

Natsu Asami, Sarasa Yano, Fuminori Tsuruta

Abstract read
In one paragraph

Article in microPublication biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

3 authors.

Natsu AsamiMaster's Program in Biology, Degree Programs in Life and Earth Sciences, Graduate School of Science and Technology, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan.
Sarasa YanoGraduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan.
Fuminori TsurutaMaster's and Doctoral Program in Biology, Institute of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Micronuclei (MN) serve as well-established markers of genomic instability. MN arise from various stresses, such as segregation errors and mechanical stress, and are subsequently eliminated by the autophagy pathway. It has been suggested that MN are traditionally considered markers of cancer cells, often without recognized functional significance. Meanwhile, we recently discovered that MN act as mediators in regulating microglial characteristics. Neurons produce MN in response to migrating stress during the developmental stage and release them to the extracellular space, subsequently transferring them to microglia. In this study, we report the potential mechanisms underlying MN release through the autophagic secretion pathway. Our data show a possibility by which damaged MN are recognized autophagy regulatory factors, resulting in the propagation of MN to microglia.

Identifiers

PMID40134942
PMCPMC11933925

What OpenQuestion holds

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LicenceCC BY
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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.