Evidence map›Paper›PMID 31035067›Full record

ArticleJournal of the mechanical behavior of biomedical materials2019

Bioengineered analog of stromal cell-derived factor 1α preserves the biaxial mechanical properties of native myocardium after infarction.

Hanjay Wang, Andrew Wisneski, Michael J Paulsen, Annabel Imbrie-Moore, Zhongjie Wang, Yue Xuan, Hector Lopez Hernandez, Haley J Lucian, Anahita Eskandari, Akshara D Thakore and 9 more

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

Article in Journal of the mechanical behavior of biomedical materials, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Article
  6. Navigating the Crossroads of Cell Therapy and Natural Heart Regeneration.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Article
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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

19 authors at 2 institutions in 1 country.

Hanjay WangDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Andrew WisneskiDepartment of Surgery, University of California San Francisco, San Francisco, CA, USA.
Michael J PaulsenDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Annabel Imbrie-MooreDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA; Department of Mechanical Engineering, Stanford University, Stanford, CA, USA.
Zhongjie WangDepartment of Surgery, University of California San Francisco, San Francisco, CA, USA.
Yue XuanDepartment of Surgery, University of California San Francisco, San Francisco, CA, USA.
Hector Lopez HernandezDepartment of Materials Science and Engineering, Stanford University, Stanford, CA, USA.
Haley J LucianDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Anahita EskandariDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Akshara D ThakoreDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Justin M FarryDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Camille E HironakaDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Daniel von BornstaedtDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Amanda N SteeleDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA; Department of Bioengineering, Stanford University, Stanford, CA, USA.
Lyndsay M StapletonDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA; Department of Bioengineering, Stanford University, Stanford, CA, USA.
Kiah M WilliamsDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Matthew A WuDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
John W MacArthurDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA.
Y Joseph WooDepartment of Cardiothoracic Surgery, Stanford University, Stanford, CA, USA; Department of Bioengineering, Stanford University, Stanford, CA, USA. Electronic address: joswoo@stanford.edu.
Stanford University · USUniversity of California, San Francisco · US

Funding

ANGIOGENIC TISSUE ENGINEERING TO LIMIT POST-INFARCTION VENTRICULAR REMODELINGR01HL089315 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI WOO, Y JOSEPH · 2008 to 2023
$6.4M
American Heart Association-American Stroke Association 17POST33410497American Heart Association-American Stroke Association 18POST33990223NHLBI NIH HHS R01 HL089315
6 · The paper itself

Abstract

Adverse remodeling of the left ventricle (LV) after myocardial infarction (MI) results in abnormal tissue biomechanics and impaired cardiac function, often leading to heart failure. We hypothesized that intramyocardial delivery of engineered stromal cell-derived factor 1α analog (ESA), our previously-developed supra-efficient pro-angiogenic chemokine, preserves biaxial LV mechanical properties after MI. Male Wistar rats (n = 45) underwent sham surgery (n = 15) or permanent left anterior descending coronary artery ligation. Rats sustaining MI were randomized for intramyocardial injections of either saline (100 μL, n = 15) or ESA (6 μg/kg, n = 15), delivered at four standardized borderzone sites. After 4 weeks, echocardiography was performed, and the hearts were explanted. Tensile testing of the anterolateral LV wall was performed using a displacement-controlled biaxial load frame, and modulus was determined after constitutive modeling. At 4 weeks post-MI, compared to saline controls, ESA-treated hearts had greater wall thickness (1.68 ± 0.05 mm vs 1.42 ± 0.08 mm, p = 0.008), smaller end-diastolic LV internal dimension (6.88 ± 0.29 mm vs 7.69 ± 0.22 mm, p = 0.044), and improved ejection fraction (62.8 ± 3.0% vs 49.4 ± 4.5%, p = 0.014). Histologic analysis revealed significantly reduced infarct size for ESA-treated hearts compared to saline controls (29.4 ± 2.9% vs 41.6 ± 3.1%, p = 0.021). Infarcted hearts treated with ESA exhibited decreased modulus compared to those treated with saline in both the circumferential (211.5 ± 6.9 kPa vs 264.3 ± 12.5 kPa, p = 0.001) and longitudinal axes (194.5 ± 6.5 kPa vs 258.1 ± 14.4 kPa, p < 0.001). In both principal directions, ESA-treated infarcted hearts possessed similar tissue compliance as sham non-infarcted hearts. Overall, intramyocardial ESA therapy improves post-MI ventricular remodeling and function, reduces infarct size, and preserves native LV biaxial mechanical properties.

Indexed as

Protein EngineeringAnimalsBiomechanical PhenomenaChemokine CXCL12HeartMaleMechanical PhenomenaMyocardial InfarctionRatsRats, WistarVentricular RemodelingChemokine CXCL12Angiogenic therapyBiaxial tensionMyocardial infarctionVentricular remodeling

Identifiers

PMID31035067
PMCPMC6701187
OpenAlexW2937333635

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.