Evidence map›Paper›PMID 40229986›Full record

ArticleStem cells (Dayton, Ohio)2025

Newborn apical resection preserves the proliferative capacity of cardiomyocytes located throughout the left ventricle.

Kaili Hao, Thanh Nguyen, Yuji Nakada, Gregory Walcott, Yuhua Wei, Yalin Wu, Daniel J Garry, Peng Yao, Jianyi Zhang

Abstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Kaili HaoDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Thanh NguyenDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, United States.ORCID 0000-0002-8440-1594
Yuji NakadaDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Gregory WalcottDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Yuhua WeiDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Yalin WuDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Daniel J GarryDepartment of Medicine, School of Medicine, University of Minnesota, Minneapolis, MN 55455, United States.ORCID 0000-0002-8970-7365
Peng YaoAab Cardiovascular Research Institute, Department of Biochemistry & Biophysics, The Center for RNA Biology, School of Medicine, University of Rochester, Rochester, NY 14642, United States.ORCID 0000-0002-1145-3967
Jianyi ZhangDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, United States.ORCID 0000-0002-3955-6554

Funding

Project 3 - Role of Proline Metabolism in Regulation of Mammalian Cardiomyocyte ProliferationP01HL160476 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Hesham Sadek · 2022 to 2026
$13.1M
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
Deciphering the Neonatal Cardiac Regenerative Potential and Regulators in Large AnimalsR01HL149137 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SADEK, HESHAM, ZANGI, LIOR · 2019 to 2022
$2.5M
uORF-mediated Translational Control of Cardiac Transcription Factor ExpressionR01HL164584 · NHLBI · UNIVERSITY OF ROCHESTER · PI Peng Yao · 2023 to 2026
$2.0M
Deciphering the role of FAM210A in cardiac physiopathologyR01HL169432 · NHLBI · UNIVERSITY OF ROCHESTER · PI Peng Yao · 2023 to 2026
$1.9M
Translational Control of Cardiac FibrosisR01HL147954 · NHLBI · UNIVERSITY OF ROCHESTER · PI YAO, PENG · 2019 to 2022
$1.5M
Role of miR-574-Fam210a axis in cardiac hypertrophy and remodelingR01HL132899 · NHLBI · UNIVERSITY OF ROCHESTER · PI YAO, PENG · 2018 to 2021
$1.5M
NHLBI NIH HHS P01 HL160476NHLBI NIH HHS R01 HL114120NHLBI NIH HHS R01 HL131017NHLBI NIH HHS R01 HL132899NHLBI NIH HHS R01 HL147954NHLBI NIH HHS R01 HL149137NHLBI NIH HHS R01 HL164584NHLBI NIH HHS R01 HL169432NHLBI NIH HHS U01 HL134764NIH HHS HL131017NIH HHS HL 149137NIH HHS HL164584NIH HHS HL169432NIH HHS NIH P01 HL160476NIH HHS NIH R01s: HL147954NIH HHS NIH U01 HL134764NIH HHS R01s: HL114120
6 · The paper itself

Abstract

backgroundWhen pigs underwent apical resection (AR) on postnatal day (P) 1 (ARP1) followed by myocardial infarction (MI) on P28, the hearts had little evidence of scarring; meanwhile, hearts underwent MI on P28 without ARP1 showed large infarcts on P56; and the improvement of ARP1 hearts was driven primarily by cardiomyocyte proliferation. AR and MI were performed ~5 mm (AR) and ~20 mm (MI) above the heart apex; thus, we hypothesize that ARP1 preserved the cardiomyocytes cell-cycle throughout the left ventricle, rather than only near the resection site.

methodsSections of cardiac tissue were collected from the left ventricle of uninjured pigs and from both the border zone (BZ) of AR and uninjured regions (remote zone, [RZ]) in ARP1 hearts. Cardiomyocyte proliferation was evaluated via immunofluorescence analysis of phosphorylated histone 3 [PH3] and symmetric Aurora B (sAuB). Single nucleus RNA sequencing (snRNAseq) data collected from the hearts of fetal pigs, uninjured pigs, and the BZ and RZ of ARP1 pigs was evaluated via our cell-cycle-specific autoencoder to identify proliferating cardiomyocytes.

resultsCardiomyocyte PH3 and sAuB expression, and percentage of proliferating cardiomyocytes in snRNA data was significantly more common in both BZ and RZ of ARP1 than uninjured hearts but did not differ significantly between the ARP1-BZ and ARP1-RZ at any time point. Heat shock proteins HSPA5 and HSP90B1 were overexpressed at both ARP1-BZ and ARP1-RZ. In AC16 cell, overexpression (and knockdown) of HSPA5-HSP90B1 increased (and decrease) cell-cycle activity.

conclusionARP1 preserved proliferative capacity of cardiomyocytes located throughout the left ventricle.

Indexed as

Heart VentriclesMyocytes, CardiacAnimalsAnimals, NewbornCell ProliferationMyocardial InfarctionSwineapical resectioncardiomyocytecell-cycleheart regenerationheat-shock protein

Identifiers

PMID40229986
PMCPMC12080357

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.