ReviewHeart failure reviews2007
Return to the fetal gene program protects the stressed heart: a strong hypothesis.
Review in Heart failure reviews, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers, 2 of them syntheses that pooled 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.
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
227 citing papers in PubMed, 2 syntheses or guidelines pooled it, 423 citations in OpenAlex.
- A systematic review of fetal genes as biomarkers of cardiac hypertrophy in rodent models of diabetes.PloS one · 2014Pooled it
- Reciprocal transcriptional regulation of metabolic and signaling pathways correlates with disease severity in heart failure.Circulation. Cardiovascular genetics · 2011Pooled it
- Therapeutic Molecular Phenotype of β-Blocker-Associated Reverse-Remodeling in Nonischemic Dilated Cardiomyopathy.Circulation. Cardiovascular genetics · 2015Trial
- A randomized pilot trial of remote ischemic preconditioning in heart failure with reduced ejection fraction.PloS one · 2014Trial
- Fast skeletal myosin binding protein-C expression exacerbates dysfunction in heart failure.Basic research in cardiology · 2026Article
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- Loss of ATP-Dependent Citrate Lyase Drives Left Ventricular Dysfunction by Metabolic Remodeling.Circulation · 2026Article
- Plasma amino acid concentrations at admission and 28-day mortality in ST-elevation myocardial infarction.Nutrition & metabolism · 2026Article
- 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
- Nanoparticle-Based Therapeutic Strategies for Pathological Cardiac Hypertrophy: Preclinical Advances, Translational Challenges, and Future Perspectives.International journal of nanomedicine · 2026Review
- Mechanism of RNA Oxidation and Its Inhibitor Involved in Ang II-Induced Cardiomyocyte Hypertrophy.Aging medicine (Milton (N.S.W)) · 2025Article
- Autonomic Imbalance in Cardiomyopathy and Heart Failure: From Neurobiology to Precision Neuromodulation.Current cardiology reports · 2025Review
- Efficacy of Contractility Modulation Therapy in Patients with Transthyretin Amyloid Cardiomyopathy, Mildly Reduced to Reduced EF and NYHA III and IV: A Multicentric, Prospective Pilot Study for AMY-CCM Registry.Journal of cardiovascular development and disease · 2025Article
- A ratiometric catalog of protein isoform shifts in the cardiac fetal gene program.JCI insight · 2025Article
- Characterization of human living myocardial slices culture-induced adaptations: a translational perspective.Journal of molecular and cellular cardiology plus · 2025Article
- Living myocardial slices: walking the path towards standardization.Cardiovascular research · 2025Review
- Differential regulation during development, aging, and disease implies heart cell specific functions of the Mediator Complex.Journal of molecular and cellular cardiology plus · 2025Article
- Thymosin Beta-4 Modulates Cardiac Remodeling by Regulating ROCK1 Expression in Adult Mammals.International journal of molecular sciences · 2025Article
- Article
- MicroRNA mediated regulation in early-onset cardiac hypertrophy: Insights from the hypertrophic heart rat model.PloS one · 2025Article
167 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
A common feature of the hemodynamically or metabolically stressed heart is the return to a pattern of fetal metabolism. A hallmark of fetal metabolism is the predominance of carbohydrates as substrates for energy provision in a relatively hypoxic environment. When the normal heart is exposed to an oxygen rich environment after birth, energy substrate metabolism is rapidly switched to oxidation of fatty acids. This switch goes along with the expression of "adult" isoforms of metabolic enzymes and other proteins. However, the heart retains the ability to return to the "fetal" gene program. Specifically, the fetal gene program is predominant in a variety of pathophysiologic conditions including hypoxia, ischemia, hypertrophy, and atrophy. A common feature of all of these conditions is extensive remodeling, a decrease in the rate of aerobic metabolism in the cardiomyocyte, and an increase in cardiac efficiency. The adaptation is associated with a whole program of cell survival under stress. The adaptive mechanisms are prominently developed in hibernating myocardium, but they are also a feature of the failing heart muscle. We propose that in failing heart muscle at a certain point the fetal gene program is no longer sufficient to support cardiac structure and function. The exact mechanisms underlying the transition from adaptation to cardiomyocyte dysfunction are still not completely understood.
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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.