Evidence map›Paper›PMID 39799185›Full record

ArticleNPJ Regenerative medicine2025

Pharmacological or genetic inhibition of LTCC promotes cardiomyocyte proliferation through inhibition of calcineurin activity.

Lynn A C Devilée, Abou Bakr M Salama, Jessica M Miller, Janice D Reid, Qinghui Ou, Nourhan M Baraka, Kamal Abou Farraj, Madiha Jamal, Yibing Nong, Todd K Rosengart and 5 more

Abstract read
In one paragraph

Article in NPJ Regenerative medicine, 2025. 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
–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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Advances in Drug Discovery for Cardiomyocyte Proliferation.Current treatment options in cardiovascular medicine · 2025
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Lynn A C DeviléeQIMR Berghofer Medical Research Institute, Cardiac Bioengineering Laboratory, Brisbane, Australia.ORCID http://orcid.org/0000-0002-6176-4392
Abou Bakr M SalamaInstitute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, USA.ORCID http://orcid.org/0000-0002-2241-3792
Jessica M MillerInstitute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, USA.
Janice D ReidQIMR Berghofer Medical Research Institute, Cardiac Bioengineering Laboratory, Brisbane, Australia.
Qinghui OuInstitute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, USA.
Nourhan M BarakaSurgery Department, Baylor College of Medicine, Houston, USA.
Kamal Abou FarrajSurgery Department, Baylor College of Medicine, Houston, USA.
Madiha JamalInstitute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, USA.
Yibing NongCenter for Cardiometabolic Science, Christina Lee Brown Envirome Institute, Department of Medicine, University of Louisville, Louisville, USA.ORCID http://orcid.org/0000-0001-7934-7821
Todd K RosengartSurgery Department, Baylor College of Medicine, Houston, USA.
Douglas AndresDepartment of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine, Lexington, USA.
Jonathan SatinDepartment of Physiology, University of Kentucky College of Medicine, Lexington, USA.
Tamer M A MohamedInstitute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, USA.
James E HudsonQIMR Berghofer Medical Research Institute, Cardiac Bioengineering Laboratory, Brisbane, Australia. James.Hudson@qimrberghofer.edu.au.ORCID http://orcid.org/0000-0003-0832-9356
Riham R E AbouleisaInstitute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, USA. riham.abouleisa@bcm.edu.ORCID http://orcid.org/0000-0001-8883-068X

Funding

UM1HG006348: Cas9 Genome Integrity Supplemental ProposalUM1HG006348 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI Jason D. Heaney, Chih-Wei Logan Hsu · 2016 to 2026
$47.5M
TBDP30GM127607 · NIGMS · UNIVERSITY OF LOUISVILLE · PI HILL, BRADFORD GUY · 2018 to 2022
$6.3M
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
Noradrenergic mechanisms in breathing and respiratory pathophysiologiesR01HL130249 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI RAY, RUSSELL S · 2016 to 2024
$5.3M
METABOLIC IMPACTS OF TYPE II INTERFERON SIGNALS IN OBESITYR01DK114356 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI HARTIG, SEAN · 2017 to 2025
$4.6M
Mechanisms of L-type Calcium Channel Regulation in Heart Health and DiseaseR01HL166280 · NHLBI · UNIVERSITY OF KENTUCKY · PI Jonathan Satin · 2023 to 2026
$2.5M
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
Triple Gene Therapy for Ischemic Heart FailureR61HL177472 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MOHAMED, TAMER M A, ROSENGART, TODD K · 2025 to 2025
$560k
Physiologically relevant cardiac tissue culture model for drug testing and disease modelingR15HL168688 · NHLBI · UNIVERSITY OF LOUISVILLE · PI GIRIDHARAN, GURUPRASAD A · 2023 to 2023
$464k
Vevo 3100 Ultrasound SystemS10OD032380 · OD · BAYLOR COLLEGE OF MEDICINE · PI WARD, CHRISTOPHER S · 2022 to 2022
$312k
Deciphering the Relationship Between Cardiomyocyte Metabolic Configuration and Cell Cycle Re-entryF32HL149140 · NHLBI · UNIVERSITY OF LOUISVILLE · PI ABOULEISA, RIHAM RAAFAT ELGHARIB · 2020 to 2023
$243k
American Heart Association (American Heart Association, Inc.) 16SDG29950012NHGRI NIH HHS UM1 HG006348NHLBI NIH HHS F32 HL149140NHLBI NIH HHS R01 HL130249NHLBI NIH HHS R01 HL147921NHLBI NIH HHS R01 HL166280NHLBI NIH HHS R01 HL178610NHLBI NIH HHS R15 HL168688NHLBI NIH HHS R61 HL177472NIDDK NIH HHS R01 DK114356NIGMS NIH HHS P30 GM127607NIH HHS S10 OD032380U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) P30GM127607U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL147921
6 · The paper itself

Abstract

Cardiomyocytes (CMs) lost during ischemic cardiac injury cannot be replaced due to their limited proliferative capacity. Calcium is an important signal transducer that regulates key cellular processes, but its role in regulating CM proliferation is incompletely understood. Here we show a robust pathway for new calcium signaling-based cardiac regenerative strategies. A drug screen targeting proteins involved in CM calcium cycling in human embryonic stem cell-derived cardiac organoids (hCOs) revealed that only the inhibition of L-Type Calcium Channel (LTCC) induced the CM cell cycle. Furthermore, overexpression of Ras-related associated with Diabetes (RRAD), an endogenous inhibitor of LTCC, induced CM cell cycle activity in vitro, in human cardiac slices, and in vivo. Mechanistically, LTCC inhibition by RRAD or nifedipine induced CM cell cycle by modulating calcineurin activity. Moreover, ectopic expression of RRAD/CDK4/CCND in combination induced CM proliferation in vitro and in vivo, improved cardiac function and reduced scar size post-myocardial infarction.

Identifiers

PMID39799185
PMCPMC11724930

What Socratic 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 Socratic graph.