Evidence map›Paper›PMID 41285815›Full record

ArticleNature communications2025

Transient overexpression of hPKM2 in porcine cardiomyocytes prevents heart failure after myocardial infarction.

Jiacheng Sun, Yalin Wu, Matthew Adjmi, Rachel C Matthews, Ann Anu Kurian, Magdalena M Żak, Jimeen Yoo, Gayatri Mainkar, Hannah Lawless, Yu-An Lu and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Mechanisms and Therapeutic Potential of Human Cardiomyocyte Proliferation.Journal of cardiovascular development and disease · 2026
    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

15 authors.

Jiacheng Sun *Department of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL, USA.
Yalin Wu *Department of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL, USA.
Matthew Adjmi *Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Rachel C MatthewsDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL, USA.ORCID http://orcid.org/0000-0002-7339-2207
Ann Anu KurianCardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Magdalena M ŻakCardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Jimeen YooCardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Gayatri MainkarCardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Hannah LawlessDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL, USA.
Yu-An LuDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL, USA.
Patrick Soon-ShiongNantRNA, LLC, Wilmington, DE, USA.
Gregory P WalcottDivision of Cardiovascular Diseases, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
Hesham A SadekDivision of Cardiology, The University of Arizona College of Medicine, Tucson, AZ, USA.ORCID http://orcid.org/0000-0002-4745-366X
Jianyi ZhangDepartment of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham, Birmingham, AL, USA. jayzhang@uab.edu.ORCID http://orcid.org/0000-0002-3955-6554
Lior ZangiCardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA. lior.zangi@mssm.edu.ORCID http://orcid.org/0000-0002-6153-9857

Funding

Project 3 - Role of Proline Metabolism in Regulation of Mammalian Cardiomyocyte ProliferationP01HL160476 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Jianyi Zhang · 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
Induction of Cardiomyocyte Proliferation via Transient Expression of Cell Cycle Factors as a Promising Therapy for Heart FailureR01HL147921 · NHLBI · UNIVERSITY OF LOUISVILLE · PI Tamer M A Mohamed, Jonathan Satin · 2020 to 2026
$5.3M
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
Cardiomyocyte-specific modified mRNA of Pkm2 for induction of cardiac regeneration in ischemic heart failureR01HL142768 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZANGI, LIOR · 2018 to 2022
$2.1M
Defining the major signaling mechanism which controls spontaneous cardiomyocyte proliferation in the Neonatal StageR01HL178610 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Tamer M A Mohamed · 2025 to 2026
$1.5M
NHLBI NIH HHS P01 HL160476NHLBI NIH HHS R01 HL114120NHLBI NIH HHS R01 HL131017NHLBI NIH HHS R01 HL142768NHLBI NIH HHS R01 HL147921NHLBI NIH HHS R01 HL149137NHLBI NIH HHS R01 HL178610NHLBI NIH HHS U01 HL134764U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01 HL142768-01U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01 HL149137-01
6 · The paper itself

Abstract

The adult mammalian heart lacks the ability to regenerate after injury, contributing to heart failure. No current treatment reactivates heart muscle cell division to prevent this decline. We used a targeted, non-viral modified mRNA system to transiently boost expression of a regenerative enzyme, pyruvate kinase muscle isozyme M2, in heart muscle cells of juvenile and adult pig models after ischemic injury. In juvenile pigs treated one-week post-injury, we observed increased markers of cell division, secretion of protective factors, improved heart function, and reduced scarring two months later. In adult pigs treated immediately after injury, we saw improved heart contractility and less fibrosis one month later. These results show that targeted pyruvate kinase muscle isozyme M2 modified mRNA delivery can stimulate muscle regeneration and functional recovery in both young and adult pig hearts. This approach offers a promising strategy for repairing ischemic injury and preventing heart failure in humans.

Indexed as

Heart FailureMyocardial InfarctionMyocytes, CardiacPyruvate KinaseAnimalsDisease Models, AnimalMyocardiumRegenerationRNA, MessengerSwinePyruvate KinaseRNA, Messenger

Identifiers

PMID41285815
PMCPMC12645031

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.