Evidence map›Paper›PMID 32838837›Full record

ArticleeLife2020

Identification of specific Tie2 cleavage sites and therapeutic modulation in experimental sepsis.

Temitayo O Idowu, Valerie Etzrodt, Benjamin Seeliger, Patricia Bolanos-Palmieri, Kristina Thamm, Hermann Haller, Sascha David

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 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 31% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Aflibercept and Faricimab Equipotently Restore Endothelial Barrier Function.Investigative ophthalmology & visual science · 2026
    Article
  4. Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target.Journal of cellular and molecular medicine · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Flow-dependent regulation of endothelial Tie2 by GATA3 in vivo.Intensive care medicine experimental · 2021
    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

7 authors at 1 institution in 2 countries.

Temitayo O IdowuDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.ORCID 0000-0002-3321-8589
Valerie EtzrodtDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Benjamin SeeligerDepartment of Respiratory Medicine and German Centre of Lung Research (DZL), Hannover Medical School, Hannover, Germany.
Patricia Bolanos-PalmieriDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Kristina ThammDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Hermann HallerDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Sascha DavidDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.ORCID 0000-0002-8231-0461
Medizinische Hochschule Hannover · DE

Funding

Deutsche Forschungsgemeinschaft DA1209/4-3
6 · The paper itself

Abstract

Endothelial Tie2 signaling plays a pivotal role in vascular barrier maintenance at baseline and after injury. We previously demonstrated that a sharp drop in Tie2 expression observed across various murine models of critical illnesses is associated with increased vascular permeability and mortality. Matrix metalloprotease (MMP)-14-mediated Tie2 ectodomain shedding has recently been recognized as a possible mechanism for Tie2 downregulation in sepsis. Here, we identified the exact MMP14-mediated Tie2 ectodomain cleavage sites and could show that pharmacological MMP14 blockade in experimental murine sepsis exerts barrier protective and anti-inflammatory effects predominantly through the attenuation of Tie2 cleavage to improve survival both in a pre-treatment and rescue approach. Overall, we show that protecting Tie2 shedding might offer a new therapeutic opportunity for the treatment of septic vascular leakage.

Indexed as

Receptor, TIE-2SepsisAnimalsCapillary PermeabilityDisease Models, AnimalFibronectin Type III DomainHumansHuman Umbilical Vein Endothelial CellsMaleMatrix Metalloproteinase 14Matrix Metalloproteinase InhibitorsMiceMice, Inbred C57BLSignal TransductionMatrix Metalloproteinase 14Matrix Metalloproteinase InhibitorsReceptor, TIE-2TEK protein, humanTek protein, mouseendothelial cellsimmunologyinflammationmedicineMMP14mousepermeabilitySepsisTie2vascular barrier function

Identifiers

PMID32838837
PMCPMC7447424
OpenAlexW3080584368

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.