Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Can the cardiomyocyte cell cycle be reprogrammed?

Katrina A Bicknell1, Carmen H Coxon, Gavin Brooks

  • 1School of Pharmacy, University of Reading, PO Box 226 Whiteknights, Reading Berkshire RG6 6AP, UK. k.bicknell@reading.ac.uk

Journal of Molecular and Cellular Cardiology
|March 17, 2007
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Phages for One Health: regulatory and product life cycle considerations.

Microbiology (Reading, England)·2026
Same author

Structural basis for inhibition of coagulation factor VIII reveals a shared antigenic hotspot on the C1 domain.

Journal of thrombosis and haemostasis : JTH·2024
Same author

Reproducibility and Harmonization in Research using Biological Standards: The Example of Platelet Agonist Collagen-Related Peptide.

Journal of visualized experiments : JoVE·2023
Same author

Structure of coagulation factor VIII bound to a patient-derived anti-C1 domain antibody inhibitor.

Blood·2023
Same author

Characterisation and application of recombinant FVIII-neutralising antibodies from haemophilia A inhibitor patients.

British journal of haematology·2021
Same author

FVIII inhibitors display FV-neutralizing activity in the prothrombin time assay.

Journal of thrombosis and haemostasis : JTH·2021
Same journal

Large extracellular vesicles derived from red blood cells in coronary artery disease patients with anemia promote endothelial dysfunction.

Journal of molecular and cellular cardiology·2026
Same journal

SnRNA-seq identifies FN1-SDC4 axis triggering epicardial activation in right ventricular remodeling in pulmonary hypertension.

Journal of molecular and cellular cardiology·2026
Same journal

Therapeutic impact of normal dietary patterns on diabetic cardiomyopathy: Transcriptomic and proteomic insights.

Journal of molecular and cellular cardiology·2026
Same journal

Structural, biophysical and cellular assessment of filamin C M82K: A test case for VUS interpretation in cardiomyopathy.

Journal of molecular and cellular cardiology·2026
Same journal

Precision modification of heart failure signaling by CRISPR-Cas9 base editing.

Journal of molecular and cellular cardiology·2026
Same journal

Retraction notice to 'Sam68 impedes the recovery of arterial injury by augmenting inflammatory response' [Journal of Molecular and Cellular Cardiology 137 (2019) 82-92].

Journal of molecular and cellular cardiology·2026
See all related articles

Adult cardiomyocytes lose their ability to proliferate after birth, limiting cardiac repair. Understanding cardiomyocyte cell cycle regulation may reveal new therapeutic targets for heart injury recovery.

Area of Science:

  • Cardiovascular Biology
  • Cell Cycle Regulation
  • Regenerative Medicine

Background:

  • Adult cardiomyocytes have limited proliferative capacity, hindering cardiac repair after myocardial injury.
  • Cardiomyocyte cell cycle withdrawal and differentiation occur early in mammalian development.
  • Mechanisms governing cardiomyocyte cell cycle exit are not fully understood, representing a gap in knowledge for therapeutic development.

Purpose of the Study:

  • To review the current understanding of cardiomyocyte cell cycle regulation.
  • To summarize recent findings on manipulating cell cycle regulators in cardiomyocytes.
  • To discuss the potential of therapeutic strategies aimed at restoring cardiomyocyte proliferation for cardiac repair.

Main Methods:

  • Review of existing literature on cardiomyocyte cell cycle control.

Related Experiment Videos

  • Analysis of studies using transgenic mouse models and recombinant adenoviruses.
  • Examination of in vivo and in vitro manipulation of cell cycle regulators.

    • Main Results:

    • Cardiomyocyte proliferation is largely lost postnatally due to cell cycle withdrawal.
    • Research has focused on manipulating cell cycle regulators to understand their role.
    • Studies explore the feasibility of re-inducing proliferation in adult cardiomyocytes.

    Conclusions:

    • Understanding cardiomyocyte cell cycle regulation is crucial for developing therapies for myocardial injury.
    • Targeting cell cycle regulators offers potential for enhancing cardiac repair.
    • Restoring cardiomyocyte proliferative potential is a promising, albeit challenging, therapeutic strategy.