ReviewAnnual review of pathology2016
Genetics of Cardiac Developmental Disorders: Cardiomyocyte Proliferation and Growth and Relevance to Heart Failure.
Review in Annual review of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed.
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Single-Cell Multi-Omics Reveal Gene Regulatory Mechanisms Underlying Cardiac Embryonic Development.Genes · 2026Review
- IRX4204 sensitizes multiple myeloma to ferroptosis and improves lenalidomide efficacy through the HMOX1-GPX4 axis.Scientific reports · 2026Article
- Allogeneic, Xenogeneic, and Exogenic Hearts for Transplantation.Methodist DeBakey cardiovascular journal · 2025Review
- Non-compaction of the ventricular myocardium associated with large patent ductus arteriosus: primary or secondary?BMC cardiovascular disorders · 2024Article
- Determination of Genotype and Phenotypes in Pediatric Patients With Biventricular Noncompaction.Journal of the American Heart Association · 2024Article
- Frameshift variants in C10orf71 cause dilated cardiomyopathy in human, mouse, and organoid models.The Journal of clinical investigation · 2024Article
- The changing morphology of the ventricular walls of mouse and human with increasing gestation.Journal of anatomy · 2024Article
- Cardiac manifestations of human ACTA2 variants recapitulated in a zebrafish model.Journal of human genetics · 2024Article
- SGLT2 inhibition, venous thrombolism, and death due to cardiac causes: a mediation Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- Molecular Pathways and Animal Models of Ebstein's Anomaly.Advances in experimental medicine and biology · 2024Review
- Omentin-1 drives cardiomyocyte cell cycle arrest and metabolic maturation by interacting with BMP7.Cellular and molecular life sciences : CMLS · 2023Article
- Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway.Scientific reports · 2023Article
- Networks that Govern Cardiomyocyte Proliferation to Facilitate Repair of the Injured Mammalian Heart.Methodist DeBakey cardiovascular journal · 2023Review
- WDR62 variants contribute to congenital heart disease by inhibiting cardiomyocyte proliferation.Clinical and translational medicine · 2022Article
- Left Ventricular Noncompaction in Children: The Role of Genetics, Morphology, and Function for Outcome.Journal of cardiovascular development and disease · 2022Review
- RBPMS is an RNA-binding protein that mediates cardiomyocyte binucleation and cardiovascular development.Developmental cell · 2022Article
- Higher spatial resolution improves the interpretation of the extent of ventricular trabeculation.Journal of anatomy · 2022Article
- Endocardial-Myocardial Interactions During Early Cardiac Differentiation and Trabeculation.Frontiers in cardiovascular medicine · 2022Review
- Case Report: First Case of Non-restrictive Ventricular Septal Defect With Congestive Heart Failure in a Chinese Han Male Infant Carrying a Class II Chromosome 17p13.3 Microduplication.Frontiers in pediatrics · 2022Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Cardiac developmental disorders represent the most common of human birth defects, and anomalies in cardiomyocyte proliferation drive many of these disorders. This review highlights the molecular mechanisms of prenatal cardiac growth. Trabeculation represents the initial ventricular growth phase and is necessary for embryonic survival. Later in development, the bulk of the ventricular wall derives from the compaction process, yet the arrest of this process can still be compatible with life. Cardiomyocyte proliferation and growth form the basis of both trabeculation and compaction, and mouse models indicate that cardiomyocyte interactions with the surrounding environment are critical for these proliferative processes. The human genetics of left ventricular noncompaction cardiomyopathy suggest that cardiomyocyte cell-autonomous mechanisms contribute to the compaction process. Understanding the determinants of prenatal or early postnatal cardiomyocyte proliferation and growth provides critical information that identifies risk factors for cardiovascular disease, including heart failure and its associated complications of arrhythmias and thromboembolic events.
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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.