Evidence map›Paper›PMID 31350544›Full record

ArticleCardiovascular research2020

N-cadherin overexpression enhances the reparative potency of human-induced pluripotent stem cell-derived cardiac myocytes in infarcted mouse hearts.

Xi Lou, Meng Zhao, Chengming Fan, Vladimir G Fast, Mani T Valarmathi, Wuqiang Zhu, Jianyi Zhang

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

Article in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 3 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Cellular Mechanisms Enabling Mitochondria Transfer and Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  5. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
  6. Pluripotent stem cell-based approaches for heart repair and the potential of genetic modifications.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
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  20. MAPK/ERK Pathway as a Central Regulator in Vertebrate Organ Regeneration.International journal of molecular sciences · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Xi LouDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall G094J, Birmingham, AL 35294, USA.
Meng ZhaoDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall G094J, Birmingham, AL 35294, USA.
Chengming FanDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall G094J, Birmingham, AL 35294, USA.
Vladimir G FastDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall G094J, Birmingham, AL 35294, USA.
Mani T ValarmathiDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall G094J, Birmingham, AL 35294, USA.
Wuqiang ZhuDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall G094J, Birmingham, AL 35294, USA.
Jianyi ZhangDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall G094J, Birmingham, AL 35294, USA.
University of Alabama at Birmingham · US

Funding

Integrated Cellular and Tissue Engineering for Ischemic Heart DiseaseU01HL134764 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BURSAC, NENAD, KAMP, TIMOTHY J. · 2016 to 2022
$7.7M
Supplement of HL131017: Myocardial remuscularization by cardiac patch delivery of epicardial FSTL1 and CCND2 overexpressing cardiomyocytesR01HL131017 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SERPOOSHAN, VAHID, ZHANG, JIANYI · 2016 to 2025
$5.8M
Endogenous and exogenous mechanisms that promote myocardial remuscularization in post infarction LV remodelingR01HL114120 · NHLBI · UNIVERSITY OF MINNESOTA · PI ZHANG, JIANYI · 2012 to 2021
$5.6M
Myocardial Repair with a Novel Engineered Cardiac Muscle PatchR01HL142627 · NHLBI · MAYO CLINIC ARIZONA · PI ZHU, WUQIANG · 2019 to 2022
$1.7M
Myocardial Repair with a Novel Engineered Cardiac Muscle PatchR56HL142627 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHU, WUQIANG · 2018 to 2018
$371k
NHLBI NIH HHS R01 HL114120NHLBI NIH HHS R01 HL131017NHLBI NIH HHS R01 HL142627NHLBI NIH HHS R56 HL142627NHLBI NIH HHS U01 HL134764
6 · The paper itself

Abstract

aimsIn regenerative medicine, cellular cardiomyoplasty is one of the promising options for treating myocardial infarction (MI); however, the efficacy of such treatment has shown to be limited due to poor survival and/or functional integration of implanted cells. Within the heart, the adhesion between cardiac myocytes (CMs) is mediated by N-cadherin (CDH2) and is critical for the heart to function as an electromechanical syncytium. In this study, we have investigated whether the reparative potency of human-induced pluripotent stem cell-derived cardiac myocytes (hiPSC-CMs) can be enhanced through CDH2 overexpression. METHODS AND

resultsCDH2-hiPSC-CMs and control wild-type (WT)-hiPSC-CMs were cultured in myogenic differentiation medium for 28 days. Using a mouse MI model, the cell survival/engraftment rate, infarct size, and cardiac functions were evaluated post-MI, at Day 7 or Day 28. In vitro, conduction velocities were significantly greater in CDH2-hiPSC-CMs than in WT-hiPSC-CMs. While, in vivo, measurements of cardiac functions: left ventricular (LV) ejection fraction, reduction in infarct size, and the cell engraftment rate were significantly higher in CDH2-hiPSC-CMs treated MI group than in WT-hiPSC-CMs treated MI group. Mechanistically, paracrine activation of ERK signal transduction pathway by CDH2-hiPSC-CMs, significantly induced neo-vasculogenesis, resulting in a higher survival of implanted cells.

conclusionCollectively, these data suggest that CDH2 overexpression enhances not only the survival/engraftment of cultured CDH2-hiPSC-CMs, but also the functional integration of these cells, consequently, the augmentation of the reparative properties of implanted CDH2-hiPSC-CMs in the failing hearts.

Indexed as

RegenerationAction PotentialsAnimalsAntigens, CDApoptosisCadherinsCell DifferentiationCell LineDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesHumansInduced Pluripotent Stem CellsMice, Inbred NODMice, SCIDMyocardial InfarctionMyocardiumAntigens, CDCadherinsCDH2 protein, humanExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktCardiac myocytesCardiac regenerationElectro-mechanical syncytiumHuman-induced pluripotent stem cellsMyocardial infarctionN-cadherin

Identifiers

PMID31350544
PMCPMC8204485
OpenAlexW2966328248

What Socratic 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 Socratic graph.