Evidence map›Paper›PMID 29096622›Full record

ArticleCardiovascular diabetology2017

Tissue-engineered smooth muscle cell and endothelial progenitor cell bi-level cell sheets prevent progression of cardiac dysfunction, microvascular dysfunction, and interstitial fibrosis in a rodent model of type 1 diabetes-induced cardiomyopathy.

Masashi Kawamura, Michael J Paulsen, Andrew B Goldstone, Yasuhiro Shudo, Hanjay Wang, Amanda N Steele, Lyndsay M Stapleton, Bryan B Edwards, Anahita Eskandari, Vi N Truong and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

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  19. Stem Cell Therapies in Cardiovascular Disease.Journal of cardiothoracic and vascular anesthesia · 2019
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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

15 authors at 2 institutions in 2 countries.

Masashi KawamuraDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Michael J PaulsenDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Andrew B GoldstoneDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Yasuhiro ShudoDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Hanjay WangDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Amanda N SteeleDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Lyndsay M StapletonDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Bryan B EdwardsDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Anahita EskandariDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Vi N TruongDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Kevin J JaatinenDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Arnar B IngasonDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Shigeru MiyagawaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, 565-0871, Japan.
Yoshiki SawaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, 565-0871, Japan.
Y Joseph WooDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA. joswoo@stanford.edu.
Stanford University · USOsaka University · JP

Funding

ANGIOGENIC TISSUE ENGINEERING TO LIMIT POST-INFARCTION VENTRICULAR REMODELINGR01HL089315 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI WOO, Y JOSEPH · 2008 to 2023
$6.4M
Vevo LAZR Photoacoustic and Ultrasound Imaging SystemS10OD010344 · OD · STANFORD UNIVERSITY · PI GAMBHIR, SANJIV S · 2013 to 2013
$522k
Upgrade of the Stanford GE-Varian Experimental MRI Scanner to the Current Model MS10RR026917 · NCRR · STANFORD UNIVERSITY · PI MOSELEY, MICHAEL E · 2010 to 2010
$497k
NCRR NIH HHS S10 RR026917NHLBI NIH HHS R01 HL089315NIH HHS S10 OD010344
6 · The paper itself

Abstract

backgroundDiabetes mellitus is a risk factor for coronary artery disease and diabetic cardiomyopathy, and adversely impacts outcomes following coronary artery bypass grafting. Current treatments focus on macro-revascularization and neglect the microvascular disease typical of diabetes mellitus-induced cardiomyopathy (DMCM). We hypothesized that engineered smooth muscle cell (SMC)-endothelial progenitor cell (EPC) bi-level cell sheets could improve ventricular dysfunction in DMCM.

methodsPrimary mesenchymal stem cells (MSCs) and EPCs were isolated from the bone marrow of Wistar rats, and MSCs were differentiated into SMCs by culturing on a fibronectin-coated dish. SMCs topped with EPCs were detached from a temperature-responsive culture dish to create an SMC-EPC bi-level cell sheet. A DMCM model was induced by intraperitoneal streptozotocin injection. Four weeks after induction, rats were randomized into 3 groups: control (no DMCM induction), untreated DMCM, and treated DMCM (cell sheet transplant covering the anterior surface of the left ventricle).

resultsSMC-EPC cell sheet therapy preserved cardiac function and halted adverse ventricular remodeling, as demonstrated by echocardiography and cardiac magnetic resonance imaging at 8 weeks after DMCM induction. Myocardial contrast echocardiography demonstrated that myocardial perfusion and microvascular function were preserved in the treatment group compared with untreated animals. Histological analysis demonstrated decreased interstitial fibrosis and increased microvascular density in the SMC-EPC cell sheet-treated group.

conclusionsTreatment of DMCM with tissue-engineered SMC-EPC bi-level cell sheets prevented cardiac dysfunction and microvascular disease associated with DMCM. This multi-lineage cellular therapy is a novel, translatable approach to improve microvascular disease and prevent heart failure in diabetic patients.

Indexed as

MicrovesselsAnimalsCells, CulturedDiabetes Mellitus, Type 1Diabetic CardiomyopathiesDisease Models, AnimalDisease ProgressionEndothelial Progenitor CellsFibrosisMyocytes, Smooth MuscleRatsRats, Sprague-DawleyRats, TransgenicRats, WistarRodentiaTissue EngineeringCell therapyDiabetic cardiomyopathyTissue engineering

Identifiers

PMID29096622
PMCPMC5668999
OpenAlexW2766859601

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.