Evidence map›Paper›PMID 41789122›Full record

ArticleAutophagy reports2026

Mfi2: an outer mitochondrial membrane mitofissin required for mitophagy.

Kentaro Furukawa, Tatsuro Maruyama, Yuji Sakai, Nobuo N Noda, Tomotake Kanki

Abstract read
In one paragraph

Article in Autophagy reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

5 authors.

Kentaro FurukawaDepartment of Cellular Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID https://orcid.org/0000-0002-1551-1538
Tatsuro MaruyamaInstitute of Microbial Chemistry (BIKAKEN), Tokyo, Japan.ORCID https://orcid.org/0009-0007-2550-9064
Yuji SakaiSchool of Science/Graduate School of Nanobioscience, Yokohama City University, Yokohama, Japan.ORCID https://orcid.org/0000-0002-2184-4304
Nobuo N NodaInstitute of Microbial Chemistry (BIKAKEN), Tokyo, Japan.ORCID https://orcid.org/0000-0002-6940-8069
Tomotake KankiDepartment of Cellular Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID https://orcid.org/0000-0001-9646-5379

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitophagy selectively eliminates damaged or excess mitochondria to maintain mitochondrial homeostasis. During this process, mitochondria need to be fragmented to allow their sequestration within autophagosomes. However, the well-known dynamin-related fission factors, Dnm1 in yeasts and DNM1L/DRP1 in mammals, are dispensable for mitophagy, leaving the underlying mechanism unresolved. In the yeast

Indexed as

Atg44Dnm1Mfi2mitochondrial fissionmitofissinmitophagy

Identifiers

PMID41789122
PMCPMC12959179

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.