Evidence map›Paper›PMID 25600785›Full record

ArticleCell metabolism2015

Mitochondrial fission and fusion factors reciprocally orchestrate mitophagic culling in mouse hearts and cultured fibroblasts.

Moshi Song, Katsuyoshi Mihara, Yun Chen, Luca Scorrano, Gerald W Dorn

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 320 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
320citing papers in PubMed, 1 pooled it
19.7field-weighted citation impact, top 1% 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

320 citing papers in PubMed, 1 synthesis or guideline pooled it, 473 citations in OpenAlex.

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  10. Multiscale mitochondrial cristae remodeling links Opa1 downregulation to reduced OXPHOS capacity in aged hearts.Proceedings of the National Academy of Sciences of the United States of America · 2026
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260 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 3 countries.

Moshi SongCenter for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Katsuyoshi MiharaDepartment of Molecular Biology, Kyushu University, Fukuoka 812-8582, Japan.
Yun ChenCenter for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Luca ScorranoDulbecco-Telethon Institute, Venetian Institute of Molecular Medicine and Department of Biology, University of Padua, Padova 35129, Italy.
Gerald W DornCenter for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: gdorn@dom.wustl.edu.
Washington University in St. Louis · USDulbecco Telethon Institute · ITKyushu University · JP

Funding

MOLECULAR MECHANISM OF APOPTOTIC CARDIOMYOPATHYR01HL059888 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 1999 to 2016
$5.4M
NHLBI NIH HHS HL59888NHLBI NIH HHS R01 HL059888Telethon GPP10005Telethon TCR12001
6 · The paper itself

Abstract

How mitochondrial dynamism (fission and fusion) affects mitochondrial quality control is unclear. We uncovered distinct effects on mitophagy of inhibiting Drp1-mediated mitochondrial fission versus mitofusin-mediated mitochondrial fusion. Conditional cardiomyocyte-specific Drp1 ablation evoked mitochondrial enlargement, lethal dilated cardiomyopathy, and cardiomyocyte necrosis. Conditionally ablating cardiomyocyte mitofusins (Mfn) caused mitochondrial fragmentation with eccentric remodeling and no cardiomyocyte dropout. Parallel studies in cultured murine embryonic fibroblasts (MEFs) and in vivo mouse hearts revealed that Mfn1/Mfn2 deletion provoked accumulation of defective mitochondria exhibiting an unfolded protein response, without appropriately increasing mitophagy. Conversely, interrupting mitochondrial fission by Drp1 ablation increased mitophagy and caused a generalized loss of mitochondria. Mitochondrial permeability transition pore (MPTP) opening in Drp1 null mitochondria was associated with mitophagy in MEFs and contributed to cardiomyocyte necrosis and dilated cardiomyopathy in mice. Drp1, MPTP, and cardiomyocyte mitophagy are functionally integrated. Mitochondrial fission and fusion have opposing roles during in vivo cardiac mitochondrial quality control.

Indexed as

Mitochondrial DynamicsMitophagyAnimalsCells, CulturedDynaminsFibroblastsGTP PhosphohydrolasesMiceMice, KnockoutMice, TransgenicMitochondria, HeartMyocardiumDnm1l protein, mouseDynaminsGTP PhosphohydrolasesMfn1 protein, mouseMfn2 protein, mouse

Identifiers

PMID25600785
PMCPMC4318753
OpenAlexW2044929466

What OpenQuestion holds

Textmetadata
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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.