Evidence map›Paper›PMID 23847541›Full record

ArticleFrontiers in physiology2013

Macrophages and chemokines as mediators of angiogenesis.

Jennifer L Owen, Mansour Mohamadzadeh

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 188 citations in OpenAlex.

  1. Light stimuli attenuates inflammatory activation in primary bone marrow-derived macrophages.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
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39 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 1 institution in 1 country.

Jennifer L OwenDepartment of Infectious Diseases and Pathology, Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Florida Gainesville, FL, USA.
Mansour Mohamadzadeh
University of Florida · US

Funding

UF CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR029890 · NCRR · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2009 to 2011
$14.4M
NCI NIH HHS L30 CA111002NCRR NIH HHS UL1 RR029890
6 · The paper itself

Abstract

Accumulating evidence attests to the important roles of both macrophages and chemokines in angiogenesis. Tumor-associated macrophages or TAMS constitute the major fraction of tumor-infiltrating leukocytes and are recruited by a number of chemoattractants chemoattractants that are produced by the tumor and tumor-associated stroma. This heterogeneous cell population is activated by a variety of stimuli and becomes polarized to result in functionally different phenotypes regarding tumor progression. As opposed to classically activated or M1 macrophages that exhibit anti-tumor functions, most TAMS are considered to be of the alternatively activated or M2 phenotype, and express multiple cytokines, proteases, and chemokines that promote tumor angiogenesis. Chemokines also have disparate effects on angiogenesis regulation, as several members of the CXC and CC chemokine families are potent inducers of angiogenesis, while a subset of CXC chemokines are angiostatic. This review summarizes the current literature regarding the roles and modes of action of macrophage-derived chemokines as mediators of angiogenesis.

Indexed as

angiogenesischemokine receptorschemokinesmacrophagestumor-associated macrophagestumors

Identifiers

PMID23847541
PMCPMC3701799
OpenAlexW1969847452

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.