Evidence map›Paper›PMID 32694534›Full record

ArticleNature communications2020

Mitochondrial respiration controls neoangiogenesis during wound healing and tumour growth.

L M Schiffmann, J P Werthenbach, F Heintges-Kleinhofer, J M Seeger, M Fritsch, S D Günther, S Willenborg, S Brodesser, C Lucas, C Jüngst and 10 more

Abstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed.

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  13. Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025
    Review
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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

20 authors.

L M Schiffmann *Institute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
J P Werthenbach *Institute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
F Heintges-KleinhoferInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
J M SeegerInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
M FritschInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
S D GüntherInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
S WillenborgCentre for Molecular Medicine Cologne (CMMC), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
S BrodesserLipidomics/Metabolomics Facility, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0001-5631-0663
C LucasLipidomics/Metabolomics Facility, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
C JüngstImaging Facility, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-6586-7129
M C AlbertInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
F SchornInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
A WittInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
C T MoraesDepartment of Neurology, Miller School of Medicine Miami, University of Miami, Miami, Florida, USA.
C J BrunsDepartment of General, Visceral, Cancer and Transplant Surgery, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
M PasparakisInstitute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Centre for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-9870-0966
M KrönkeInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
S A EmingCentre for Molecular Medicine Cologne (CMMC), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
O CoutelleInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
H KashkarInstitute for Medical Microbiology, Immunology and Hygiene (IMMIH), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany. h.kashkar@uni-koeln.de.ORCID http://orcid.org/0000-0003-2796-1429

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The vasculature represents a highly plastic compartment, capable of switching from a quiescent to an active proliferative state during angiogenesis. Metabolic reprogramming in endothelial cells (ECs) thereby is crucial to cover the increasing cellular energy demand under growth conditions. Here we assess the impact of mitochondrial bioenergetics on neovascularisation, by deleting cox10 gene encoding an assembly factor of cytochrome c oxidase (COX) specifically in mouse ECs, providing a model for vasculature-restricted respiratory deficiency. We show that EC-specific cox10 ablation results in deficient vascular development causing embryonic lethality. In adult mice induction of EC-specific cox10 gene deletion produces no overt phenotype. However, the angiogenic capacity of COX-deficient ECs is severely compromised under energetically demanding conditions, as revealed by significantly delayed wound-healing and impaired tumour growth. We provide genetic evidence for a requirement of mitochondrial respiration in vascular endothelial cells for neoangiogenesis during development, tissue repair and cancer.

Indexed as

Neovascularization, PhysiologicAdenosine TriphosphateAlkyl and Aryl TransferasesAnimalsCell Line, TumorCell RespirationDisease Models, AnimalEmbryo, MammalianEmbryonic DevelopmentEndothelial CellsEndothelium, VascularFemaleGene Knockout TechniquesHumansMaleMembrane ProteinsAdenosine TriphosphateAlkyl and Aryl TransferasesCOX10 protein, mouseMembrane Proteins

Identifiers

PMID32694534
PMCPMC7374592

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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.