Evidence map›Paper›PMID 32955436›Full record

ArticleeLife2020

Apelin signaling drives vascular endothelial cells toward a pro-angiogenic state.

Christian Sm Helker, Jean Eberlein, Kerstin Wilhelm, Toshiya Sugino, Julian Malchow, Annika Schuermann, Stefan Baumeister, Hyouk-Bum Kwon, Hans-Martin Maischein, Michael Potente and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
9.9field-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

76 citing papers in PubMed, 130 citations in OpenAlex.

  1. miR‑222‑3p inhibits diabetic skin wound healing by targeting APLN.International journal of molecular medicine · 2026
    Article
  2. Macrophage Dab1 Links Early Hypoxia to Adaptive Angiogenesis to Drive Peripheral Nerve Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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16 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

12 authors at 3 institutions in 1 country.

Christian Sm HelkerDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0003-0427-5338
Jean EberleinDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Kerstin WilhelmAngiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Toshiya SuginoAngiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0002-6330-7275
Julian MalchowPhilipps-University Marburg, Faculty of Biology, Cell Signaling and Dynamics, Marburg, Germany.
Annika SchuermannUniversity of Muenster, Muenster, Germany.
Stefan BaumeisterPhilipps-University Marburg, Faculty of Biology, Cell Signaling and Dynamics, Marburg, Germany.
Hyouk-Bum KwonDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Hans-Martin MaischeinDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Michael PotenteAngiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Wiebke HerzogUniversity of Muenster, Muenster, Germany.
Didier Yr StainierDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0002-0382-0026
Max Planck Institute for Heart and Lung Research · DEPhilipps University of Marburg · DEUniversity of Münster · DE

Funding

Deutsche Forschungsgemeinschaft EXC 2026Deutsche Forschungsgemeinschaft GRK2213Deutsche Forschungsgemeinschaft HE4585/3-1Deutsche Forschungsgemeinschaft SFB 834H2020 European Research Council AdG project: ZMOD 694455H2020 European Research Council EMERGE (773047)North Rhine-Westphalia return fellowship'North Rhine-Westphalia Return fellowship
6 · The paper itself

Abstract

To form new blood vessels (angiogenesis), endothelial cells (ECs) must be activated and acquire highly migratory and proliferative phenotypes. However, the molecular mechanisms that govern these processes are incompletely understood. Here, we show that Apelin signaling functions to drive ECs into such an angiogenic state. Zebrafish lacking Apelin signaling exhibit defects in endothelial tip cell morphology and sprouting. Using transplantation experiments, we find that in mosaic vessels, wild-type ECs leave the dorsal aorta (DA) and form new vessels while neighboring ECs defective in Apelin signaling remain in the DA. Mechanistically, Apelin signaling enhances glycolytic activity in ECs at least in part by increasing levels of the growth-promoting transcription factor c-Myc. Moreover,

Indexed as

AnimalsBlood VesselsChemokinesEndothelial CellsMorphogenesisSignal TransductionZebrafishZebrafish Proteinsapln protein, zebrafishChemokinesZebrafish Proteinsangiogenesisapelindevelopmental biologyendothelial cellsmetabolismnotchsproutingzebrafish

Identifiers

PMID32955436
PMCPMC7567607
OpenAlexW3087197188

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.