Evidence map›Paper›PMID 40001614›Full record

SynthesisBiomolecules2025

RNA-Binding Protein Signature in Proliferative Cardiomyocytes: A Cross-Species Meta-Analysis from Mouse, Pig, and Human Transcriptomic Profiling Data.

Thanh Nguyen, Kaili Hao, Yuji Nakada, Bijay Guragain, Peng Yao, Jianyi Zhang

Abstract readMeta-Analysis
In one paragraph

Synthesis in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

6 authors.

Thanh NguyenDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, USA.ORCID 0000-0002-8440-1594
Kaili HaoDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Yuji NakadaDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Bijay GuragainDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Peng YaoAab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.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, USA.

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
National Institute of Health R01HL114120, R01HL131017, R01HL149137, UO1HL134764, PO1HL160476, R01HL147954, R01 HL164584, R01HL169432, 24EIA1255341NHLBI 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 HL134764
6 · The paper itself

Abstract

In mammals, because cardiomyocytes withdraw from cell-cycle activities shortly after birth, the heart cannot repair the damage caused by a myocardial injury; thus, understanding how cardiomyocytes proliferate is among the most important topics in cardiovascular sciences. In newborn neonatal mammals, when a left ventricular injury is applied in hearts earlier than postnatal day 7, the cardiomyocytes actively proliferate and regenerate lost myocardium in the following weeks. The regulators promoting cardiomyocyte proliferation were discovered by analyzing transcriptomic data generated from models. Most of these regulators support the mRNA production of cell-cycle machinery, yet the mRNA requires translation into functional proteins under the regulation of RNA-binding proteins (RBPs). In this work, we performed a meta-analysis to study the relationship between RBP expression and cardiomyocyte proliferation. To identify RBPs associated with mouse and pig cardiomyocyte proliferation, the single-nuclei RNA sequencing (snRNA-seq) data from regenerating mouse and pig hearts were reanalyzed via an Autoencoder focusing on RBP expression. We also generated and analyzed new bulk RNA-seq from two human-induced pluripotent stem cell-derived (hiPSC) cardiomyocyte (hiPSC-CM) cell lines; the first cell line was harvested sixteen days after differentiation, when the cells still actively proliferated, and the second cell line was harvested one hundred and forty days after differentiation, when the cells ceased cell cycle activity. Then, the RBP associated with mouse, pig, and hiPSC-CM were compared across species. Twenty-one RBPs were found to be consistently upregulated, and six RBPs were downregulated in proliferating mouse, pig, and hiPSC-derived cardiomyocytes. Among upregulated RBPs across species, an immunofluorescence-based imaging analysis validated the significant increase in the proteins of DHX9, PTBP3, HNRNPUL1, and DDX6 in pig hearts with proliferating CMs. This meta-analysis in all species demonstrated a strong relationship between RBP expression and cardiomyocyte proliferation.

Indexed as

Myocytes, CardiacRNA-Binding ProteinsTranscriptomeAnimalsCell ProliferationGene Expression ProfilingHumansMiceSwineRNA-Binding Proteinscardiomyocytecell cycleheart regenerationRNA-binding protein

Identifiers

PMID40001614
PMCPMC11853426

What OpenQuestion holds

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Registered trials

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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.