Evidence map›Paper›PMID 36333300›Full record

ArticleNature communications2022

Mitochondrial Fission Process 1 controls inner membrane integrity and protects against heart failure.

Erminia Donnarumma, Michael Kohlhaas, Elodie Vimont, Etienne Kornobis, Thibault Chaze, Quentin Giai Gianetto, Mariette Matondo, Maryse Moya-Nilges, Christoph Maack, Timothy Wai

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

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  20. Liver kinase B1 (LKB1) regulates the epigenetic landscape of mouse pancreatic beta cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    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

10 authors at 3 institutions in 2 countries.

Erminia DonnarummaInstitut Pasteur, Mitochondrial Biology Group, CNRS UMR 3691, Université Paris Cité, Paris, France.
Michael KohlhaasDepartment of Translational Research, Comprehensive Heart Failure Center (CHFC), Medical Clinic 1, University Clinic Würzburg, Würzburg, Germany.
Elodie VimontInstitut Pasteur, Mitochondrial Biology Group, CNRS UMR 3691, Université Paris Cité, Paris, France.
Etienne KornobisInstitut Pasteur, Biomics Technological Platform, Université Paris Cité, Paris, France.ORCID 0000-0001-7712-8270
Thibault ChazeInstitut Pasteur, Proteomics Core Facility, MSBio UtechS, UAR CNRS 2024, Université Paris Cité, Paris, France.
Quentin Giai GianettoInstitut Pasteur, Bioinformatics and Biostatistics Hub, Université Paris Cité, Paris, France.
Mariette MatondoInstitut Pasteur, Proteomics Core Facility, MSBio UtechS, UAR CNRS 2024, Université Paris Cité, Paris, France.ORCID 0000-0003-3958-7710
Maryse Moya-NilgesInstitut Pasteur Ultrastructural Bio Imaging, UTechS, Université Paris Cité, Paris, France.
Christoph MaackDepartment of Translational Research, Comprehensive Heart Failure Center (CHFC), Medical Clinic 1, University Clinic Würzburg, Würzburg, Germany.ORCID 0000-0003-3694-4559
Timothy WaiInstitut Pasteur, Mitochondrial Biology Group, CNRS UMR 3691, Université Paris Cité, Paris, France. timothy.wai@pasteur.fr.ORCID 0000-0002-6770-6222
Centre National de la Recherche Scientifique · FRInstitut Pasteur · FRUniversitätsklinikum Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are paramount to the metabolism and survival of cardiomyocytes. Here we show that Mitochondrial Fission Process 1 (MTFP1) is an inner mitochondrial membrane (IMM) protein that is dispensable for mitochondrial division yet essential for cardiac structure and function. Constitutive knockout of cardiomyocyte MTFP1 in mice resulted in a fatal, adult-onset dilated cardiomyopathy accompanied by extensive mitochondrial and cardiac remodeling during the transition to heart failure. Prior to the onset of disease, knockout cardiac mitochondria displayed specific IMM defects: futile proton leak dependent upon the adenine nucleotide translocase and an increased sensitivity to the opening of the mitochondrial permeability transition pore, with which MTFP1 physically and genetically interacts. Collectively, our data reveal new functions of MTFP1 in the control of bioenergetic efficiency and cell death sensitivity and define its importance in preventing pathogenic cardiac remodeling.

Indexed as

Heart FailureMitochondrial DynamicsAnimalsMembrane ProteinsMiceMitochondria, HeartMitochondrial Membrane Transport ProteinsMyocytes, CardiacVentricular RemodelingMembrane ProteinsMitochondrial Membrane Transport Proteins

Identifiers

PMID36333300
PMCPMC9636241
OpenAlexW4308195449

What OpenQuestion 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 OpenQuestion graph.