ArticleJCI insight2019
Induction of cardiomyocyte proliferation and angiogenesis protects neonatal mice from pressure overload-associated maladaptation.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- TLR2 mediates cell cycle re-entry and survival of neonatal cardiomyocytes in response to injury.Cell communication and signaling : CCS · 2026Article
- Electrical Remodeling of Pressure Overloaded Rat Heart Is Attenuated if Imposed During Proliferative Cardiac Growth.Acta physiologica (Oxford, England) · 2025Article
- Microvascular preservation and cardiomyocyte hyperplasia underlie adaptive right ventricle development in congenital heart disease-pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2025Article
- A neonatal rat model of progressive left ventricular pressure overload induced by abdominal aortic banding microsurgery.JTCVS techniques · 2025Article
- Right ventricular volume overload reboots cardiomyocyte proliferation via immune responses.Journal of translational medicine · 2024Article
- Cauterization of the root of the left coronary artery as a straightforward, large and reproducible ischemic injury model in neonatal mice.Lab animal · 2024Review
- Hemodynamic Melody of Postnatal Cardiac and Pulmonary Development in Children with Congenital Heart Diseases.Biology · 2024Review
- Effects and mechanisms of the myocardial microenvironment on cardiomyocyte proliferation and regeneration.Frontiers in cell and developmental biology · 2024Review
- Developmental Aspects of Cardiac Adaptation to Increased Workload.Journal of cardiovascular development and disease · 2023Review
- The right ventricle in tetralogy of Fallot: adaptation to sequential loading.Frontiers in pediatrics · 2023Review
- Ability of the Right Ventricle to Serve as a Systemic Ventricle in Response to the Volume Overload at the Neonatal Stage.Biology · 2022Article
- Angiogenesis: A critical determinant for cardiac regeneration.Molecular therapy. Nucleic acids · 2022Article
- Measuring cardiomyocyte cell-cycle activity and proliferation in the age of heart regeneration.American journal of physiology. Heart and circulatory physiology · 2022Review
- Analysis of myocardial cellular gene expression during pressure overload reveals matrix based functional intercellular communication.iScience · 2022Article
- A human cell atlas of the pressure-induced hypertrophic heart.Nature cardiovascular research · 2022Article
- ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Postnatal Right Ventricular Developmental Track Changed by Volume Overload.Journal of the American Heart Association · 2021Article
- Downregulated developmental processes in the postnatal right ventricle under the influence of a volume overload.Cell death discovery · 2021Article
- TGF-β1 signaling is essential for tissue regeneration in the Xenopus tadpole tail.Biochemical and biophysical research communications · 2021Article
- Early Postnatal Cardiac Stress Does Not Influence Ventricular Cardiomyocyte Cell-Cycle Withdrawal.Journal of cardiovascular development and disease · 2021Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac pressure overload (for example due to aortic stenosis) induces irreversible myocardial dysfunction, cardiomyocyte hypertrophy and interstitial fibrosis in patients. In contrast to adult, neonatal mice can efficiently regenerate the heart after injury in the first week after birth. To decipher whether insufficient cardiac regeneration contributes to the progression of pressure overload dependent disease, we established a transverse aortic constriction protocol in neonatal mice (nTAC). nTAC in the non-regenerative stage (at postnatal day P7) induced cardiac dysfunction, myocardial fibrosis and cardiomyocyte hypertrophy. In contrast, nTAC in the regenerative stage (at P1) largely prevented these maladaptive responses and was in particular associated with enhanced myocardial angiogenesis and increased cardiomyocyte proliferation, which both supported adaptation during nTAC. A comparative transcriptomic analysis between hearts after regenerative versus non-regenerative nTAC suggested the transcription factor GATA4 as master regulator of the regenerative gene-program. Indeed, cardiomyocyte specific deletion of GATA4 converted the regenerative nTAC into a non-regenerative, maladaptive response. Our new nTAC model can be used to identify mediators of adaptation during pressure overload and to discover novel potential therapeutic strategies.
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Registered trials
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.