ReviewJournal of internal medicine2020
Cardiac foetal reprogramming: a tool to exploit novel treatment targets for the failing heart.
Review in Journal of internal medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Fast skeletal myosin binding protein-C expression exacerbates dysfunction in heart failure.Basic research in cardiology · 2026Article
- Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- An integrative single-nucleus multiomic atlas of the human left ventricle identifies gene regulatory network dynamics across cardiac development, aging, and disease.Genome biology · 2026Article
- The role of ventricular remodeling in the early decompensation of cardiorenal syndrome: Insight from studies with Ren-2 transgenic hypertensive rats subjected to volume overload induced using aorto-caval fistula.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Transcriptional regulation in heart development, disease and regeneration: reassessing the fetal gene hypothesis.Nature reviews. Cardiology · 2026Review
- The Phoenix Heart-PICSO and the Rebirth of Embryonic Life in the Ischemic Myocardium.Journal of cardiovascular development and disease · 2026Review
- Coordinated expression of BMP10/ALK1/endoglin-proteins that drive embryonic cardiac and vascular morphogenesis-in patients with heart failure: The EMPEROR Program.European journal of heart failure · 2025Article
- Matured hiPSC-derived cardiomyocytes possess dematuration plasticity.Journal of molecular and cellular cardiology plus · 2025Article
- Expression of foetal gene Pontin is essential in protecting heart against pathological remodelling and cardiomyopathy.Nature communications · 2025Article
- Exploring novel biomarkers in dilated cardiomyopathy‑induced heart failure by integrated analysis andExperimental and therapeutic medicine · 2023Article
- A role for misaligned gene expression of fetal gene program in the loss of female-specific cardiovascular protection in young obese and diabetic females.Frontiers in endocrinology · 2023Review
- ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure overload.Communications biology · 2022Article
- Programming of cardiometabolic health: the role of maternal and fetal hyperinsulinaemia.The Journal of endocrinology · 2022Review
- Study on diverse pathological characteristics of heart failure in different stages based on proteomics.Journal of cellular and molecular medicine · 2022Article
- Long-term culture of patient-derived cardiac organoids recapitulated Duchenne muscular dystrophy cardiomyopathy and disease progression.Frontiers in cell and developmental biology · 2022Article
- T3 levels and thyroid hormone signaling.Frontiers in endocrinology · 2022Review
- New Insights Into Energy Substrate Utilization and Metabolic Remodeling in Cardiac Physiological Adaption.Frontiers in physiology · 2022Review
- Selenoprotein DIO2 Is a Regulator of Mitochondrial Function, Morphology and UPRmt in Human Cardiomyocytes.International journal of molecular sciences · 2021Article
- Evidence for synergy between sarcomeres and fibroblasts in an in vitro model of myocardial reverse remodeling.Journal of molecular and cellular cardiology · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As the heart matures during embryogenesis from its foetal stages, several structural and functional modifications take place to form the adult heart. This process of maturation is in large part due to an increased volume and work load of the heart to maintain proper circulation throughout the growing body. In recent years, it has been observed that these changes are reversed to some extent as a result of cardiac disease. The process by which this occurs has been characterized as cardiac foetal reprogramming and is defined as the suppression of adult and re-activation of a foetal genes profile in the diseased myocardium. The reasons as to why this process occurs in the diseased myocardium are unknown; however, it has been suggested to be an adaptive process to counteract deleterious events taking place during cardiac remodelling. Although still in its infancy, several studies have demonstrated that targeting foetal reprogramming in heart failure can lead to substantial improvement in cardiac functionality. This is highlighted by a recent study which found that by modulating the expression of 5-oxoprolinase (OPLAH, a novel cardiac foetal gene), cardiac function can be significantly improved in mice exposed to cardiac injury. Additionally, the utilization of angiotensin receptor neprilysin inhibitors (ARNI) has demonstrated clear benefits, providing important clinical proof that drugs that increase natriuretic peptide levels (part of the foetal gene programme) indeed improve heart failure outcomes. In this review, we will highlight the most important aspects of cardiac foetal reprogramming and will discuss whether this process is a cause or consequence of heart failure. Based on this, we will also explain how a deeper understanding of this process may result in the development of novel therapeutic strategies in heart failure.
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What OpenQuestion holds
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.