Evidence map›Paper›PMID 30484107›Full record

ReviewMolecular biology reports2019

Mesenchymal stem cell dysfunction in diabetes.

Arman Fijany, Lohrasb R Sayadi, Nima Khoshab, Derek A Banyard, Ashkaun Shaterian, Michael Alexander, Johnathan R T Lakey, Keyianoosh Z Paydar, Gregory R D Evans, Alan D Widgerow

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Arman FijanyUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA.
Lohrasb R SayadiUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA.
Nima KhoshabUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA.
Derek A BanyardUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA.
Ashkaun ShaterianUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA.
Michael AlexanderUC Irvine Department of Surgery & Biomedical Engineering, Orange, CA, USA.
Johnathan R T LakeyUC Irvine Department of Surgery & Biomedical Engineering, Orange, CA, USA.
Keyianoosh Z PaydarUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA.
Gregory R D EvansUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA.
Alan D WidgerowUC Irvine Department of Plastic Surgery, Center for Tissue Engineering, Orange, CA, USA. awidgero@uci.edu.
University of California, Irvine · USUC Irvine Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) is a chronic disease that results in a variety of systemic complications. Recently, stem cell-based therapies have been proposed as potential modalities to manage DM related complications. Mesenchymal stem cell (MSC) based therapies are often considered as an ideal stem cell-based treatment for DM management due to their immunosuppressive characteristics, anti-inflammatory properties and differentiation potential. While MSCs show tremendous promise, the underlying functional deficits of MSCs in DM patients is not well understood. Using the MEDLINE database to define these functional deficits, our search yielded 1826 articles of which 33 met our inclusion criteria. This allowed us to review the topic and illuminate four major molecular categories by which MSCs are compromised in both Type 1 DM and Type II DM models which include: (1) changes in angiogenesis/vasculogenesis, (2) altered pro-inflammatory cytokine secretion, (3) increased oxidative stress markers and (4) impaired cellular differentiation and decreased proliferation. Knowledge of the deficits in MSC function will allow us to more clearly assess the efficacy of potential biologic therapies for reversing these dysfunctions when treating the complications of diabetic disease.

Indexed as

AnimalsBiomarkersCytokinesDiabetes MellitusHumansInflammation MediatorsMesenchymal Stem CellsOxidative StressBiomarkersCytokinesInflammation MediatorsDiabetesDysfunctionMesenchymal stem cellMSC

Identifiers

PMID30484107
OpenAlexW2903135877

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.