Evidence map›Paper›PMID 28582314›Full record

ReviewCurrent opinion in hematology2017

Angiopoietins and Tie2 in vascular inflammation.

Samir M Parikh

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Endotheliopathy within the thromboinflammatory network of sepsis-induced coagulopathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  10. Article
  11. Modulation of the Receptor Tyrosine Kinase TIE2/International journal of molecular sciences · 2026
    Article
  12. Article
  13. Article
  14. Review
  15. Vascular changes and their implications in lipedema.Frontiers in cell and developmental biology · 2026
    Review
  16. Article
  17. Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target.Journal of cellular and molecular medicine · 2025
    Review
  18. Review
  19. Article
  20. Article

3 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

1 author at 1 institution in 1 country.

Samir M ParikhCenter for Vascular Biology Research and Division of Nephrology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
Beth Israel Deaconess Medical Center · US

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
Simvastatin nanomedicine in ARDS and sepsisR41GM121153 · NIGMS · EUNOIA BIO TECH, LLC · PI ROBERTS, SHAWN KENNY · 2016 to 2016
$300k
NHLBI NIH HHS R01 HL093234NHLBI NIH HHS R01 HL125275NIGMS NIH HHS R41 GM121153
6 · The paper itself

Abstract

purpose of reviewAs a subset of the organism-wide reaction to severe infection, the host vascular response has received increasing attention in recent years. The transformation that small blood vessels undergo to facilitate the clearance of pathogens may become harmful to the host if it occurs too broadly or if it is sustained too long. Adverse clinical manifestations of leaky and inflamed blood vessels include edema impairing the function of critical organs and circulatory shock. RECENT

findingsThe study suggests that this host vascular response may be both measurable and potentially targetable. Tie2 is a receptor tyrosine kinase (RTK) heavily enriched in the vascular endothelium whose tonic signaling actively maintains vascular quiescence. When Tie2 becomes inactivated, important molecular brakes are released in the endothelium, which in turn potentiate inflammation and vascular leakage. The ligands of Tie2, Angiopoietin-1 and Angiopoietin-2, regulate its activation status. Genetic and molecular studies spanning thousands of humans link Tie2 and imbalance of the Angiopoietins to major adverse clinical events arising from bacterial sepsis, other severe infections, and even acute sterile inflammation. SUMMARY: The Tie2 signaling axis may constitute a molecular switch in systemic inflammation that can be measured and manipulated to target the host vascular response therapeutically.

Indexed as

Signal TransductionAngiopoietin-1Angiopoietin-2Endothelium, VascularHumansInflammationReceptor, TIE-2SepsisVasculitisAngiopoietin-1Angiopoietin-2ANGPT1 protein, humanANGPT2 protein, humanReceptor, TIE-2

Identifiers

PMID28582314
PMCPMC5777595
OpenAlexW2621307756

What OpenQuestion holds

Textmetadata
LicenceTDM
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.