Evidence map›Paper›PMID 24527350›Full record

ReviewAdvances in wound care2013

The Role of Endothelial Progenitor Cells in Postnatal Vasculogenesis: Implications for Therapeutic Neovascularization and Wound Healing.

Swathi Balaji, Alice King, Timothy M Crombleholme, Sundeep G Keswani

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Advances in wound care, 2013. 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
5.5field-weighted citation impact, top 3% 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, 161 citations in OpenAlex.

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  18. IL-10 promotes endothelial progenitor cell infiltration and wound healing via STAT3.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    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

4 authors at 1 institution in 1 country.

Swathi BalajiCenter for Molecular Fetal Therapy, Division of Pediatric, General, Thoracic, and Fetal Surgery, Cincinnati Children's Hospital and the University of Cincinnati College of Medicine , Cincinnati, Ohio.
Alice KingCenter for Molecular Fetal Therapy, Division of Pediatric, General, Thoracic, and Fetal Surgery, Cincinnati Children's Hospital and the University of Cincinnati College of Medicine , Cincinnati, Ohio.
Timothy M CrombleholmeCenter for Molecular Fetal Therapy, Division of Pediatric, General, Thoracic, and Fetal Surgery, Cincinnati Children's Hospital and the University of Cincinnati College of Medicine , Cincinnati, Ohio. ; Center for Children's Surgery, Children's Hospital Colorado and the University of Colorado School of Medicine , Aurora, Colorado.
Sundeep G KeswaniCenter for Molecular Fetal Therapy, Division of Pediatric, General, Thoracic, and Fetal Surgery, Cincinnati Children's Hospital and the University of Cincinnati College of Medicine , Cincinnati, Ohio.
Center for Children · US

Funding

Novel Mechanisms of Regenerative Fetal Wound Repair by IL-10K08GM098831 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI KESWANI, SUNDEEP G · 2011 to 2014
$480k
NIGMS NIH HHS K08 GM098831
6 · The paper itself

Abstract

significancePostnatal vasculogenesis mediated via endothelial progenitor cells (EPCs) contributes to re-endothelialization and augments neovascularization after ischemia and tissue injury, providing a novel therapeutic application. However, controversy exists with respect to the origin, identification, and contributions of the EPCs to neovascularization, necessitating further study. RECENT ADVANCES: Bone marrow (BM) or circulating cells expressing cd133/vascular endothelial growth factor receptor 2 include those with endothelial progenitor capacity. Increasing evidence suggests that there are additional BM-derived (myeloid; mesenchymal cells) and non-BM-derived (peripheral and cord-blood; tissue-resident) cell populations which also give rise to endothelial cells (ECs) and contribute to re-endothelialization and growth factor release after ischemia and tissue injury. Currently, EPCs are being used as diagnostic markers for the assessment of cardiovascular and tumor risk/progression. Techniques aimed at enhancing CRITICAL ISSUES: Mobilization and EPC-mediated neovascularization are critically regulated. Stimulatory (growth factors, statins, and exercise) or inhibitory factors (obesity, diabetes, and other cardiovascular diseases) modulate EPC numbers and function. Recruitment and incorporation of EPCs require a coordinated sequence of signaling events, including adhesion, migration (by integrins), and chemoattraction. Finally, EPCs differentiate into ECs and/or secrete angiogenic growth factors. These cells are highly plastic, and depending on the microenvironment and presence of other cells, EPCs transdifferentiate and/or undergo cell fusion and become cells of a different lineage. Therefore, FUTURE DIRECTIONS: Advances in characterization of the EPC biology and enhancement of EPC functions are required. In addition, innovative tissue-engineered carrier matrices that permit embedding of EPCs and provide optimal conditions for EPC survival and endothelial outgrowth will further contribute to EPC-mediated therapeutic applications in wound healing and ischemia repair.

Identifiers

PMID24527350
PMCPMC3751266
OpenAlexW2021693588

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.