Evidence map›Paper›PMID 25838975›Full record

ArticleTissue barriers2015

The angiopoietin-Tie2 signaling axis in the vascular leakage of systemic inflammation.

Katelyn E Milam, Samir M Parikh

Open access · bronzeAbstract read
In one paragraph

Article in Tissue barriers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

67 citing papers in PubMed, 105 citations in OpenAlex.

  1. Angiopoietin 2 Levels in the Risk Stratification and Mortality Outcome Prediction of Sepsis-Associated Coagulopathy.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018
    Trial
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  10. Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target.Journal of cellular and molecular medicine · 2025
    Review
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7 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

2 authors at 2 institutions in 2 countries.

Katelyn E MilamCenter for Vascular Biology Research; Beth Israel Deaconess Medical Center and Harvard Medical School ; Boston, MA USA.
Samir M ParikhCenter for Vascular Biology Research; Beth Israel Deaconess Medical Center and Harvard Medical School ; Boston, MA USA ; Division of Nephrology; Beth Israel Deaconess Medical Center and Harvard Medical School ; Boston, MA USA.
Center for Vascular Biology Research · USHadassah Medical Center · IL

Funding

Biology of Tie2 in sepsisR01HL093234 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PARIKH, SAMIR M · 2008 to 2017
$4.6M
Targeting the Endothelium in SepsisR01HL125275 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FLAUMENHAFT, ROBERT C, PARIKH, SAMIR M · 2014 to 2018
$4.2M
NHLBI NIH HHS R01 HL093234NHLBI NIH HHS R01 HL125275
6 · The paper itself

Abstract

The ability of small blood vessels to undergo rapid, reversible morphological changes is essential for the adaptive response to tissue injury or local infection. A canonical feature of this response is transient hyperpermeability. However, when leakiness is profound or persistent, adverse consequences accrue to the host, including organ dysfunction and shock. A growing body of literature identifies the Tie2 receptor, a transmembrane tyrosine kinase highly enriched in the endothelium, as an important regulator of vascular barrier function in health and in disease. The principal ligands of Tie2, Angiopoietins 1 and 2, exert opposite effects on this receptor in the context of inflammation. This review will focus on recent studies that have illuminated novel aspects of the exquisitely controlled Tie2 signaling axis while proposing unanswered questions and future directions for this field of study.

Indexed as

AngiopoietinAngpt, angiopoietinanthraxARDSbarrier functionEC, endothelial cellendotheliuminflammationlung injurymalariaMAPK, mitogen-activated protein kinasePI3K, phosphatidylinositol-3-kinaserespiratory distresssepsissiRNA, small interfering RNATie1Tie2vascular leakageVE-cadherin, vascular endothelial cadherinVEGF, vascular endothelial growth factorVE-PTPVE-PTP, vascular endothelial protein tyrosine phosphatase

Identifiers

PMID25838975
PMCPMC4372013
OpenAlexW1985915960

What OpenQuestion holds

Textmetadata
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.