ArticleCirculation. Heart failure2014
Energy metabolic reprogramming in the hypertrophied and early stage failing heart: a multisystems approach.
Article in Circulation. Heart failure, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 2 of them syntheses that pooled it.
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Who cites it
190 citing papers in PubMed, 2 syntheses or guidelines pooled it, 290 citations in OpenAlex.
- Reprogramming heart failure: physiological orchestration and mechanistic decoding of exercise benefits.BMC cardiovascular disorders · 2025Pooled it
- Metabolic remodeling of substrate utilization during heart failure progression.Heart failure reviews · 2019Pooled it
- Heart rate recovery as a marker of post-exercise lipid metabolism following moderate- and vigorous-intensity exercise.European journal of applied physiology · 2026Article
- Characteristics, clinical outcomes and molecular mechanisms associated with severe diastolic dysfunction in aortic stenosis.Journal of molecular and cellular cardiology plus · 2026Article
- Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Spatial imprints of emergent cardiomyocyte states in the pressure-overloaded heart.bioRxiv : the preprint server for biology · 2026Article
- TACO1 regulates mitochondrial adaptation in hypertension-induced cardiac remodeling and heart failure.Research square · 2026Article
- YY1/Asprosin/PFKP axis regulates glycolytic metabolic and exacerbates pathological cardiac hypertrophy.Nature communications · 2026Article
- Plasma and pericardial fluid metabolomic signatures of patients with ischemic heart disease.Communications medicine · 2026Article
- Targeting the undruggable transcription factor, KLF5, with a peptidomimetic small molecule, NC114, attenuates pressure overload-induced cardiac remodeling and fibrosis.Scientific reports · 2026Article
- Article
- Integrated multi-omics mapping of mitochondrial dysfunction and substrate preference in Barth syndrome cardiac tissue.EMBO molecular medicine · 2025Article
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Cardiac Ischaemia-Reperfusion Injury: Pathophysiology, Therapeutic Targets and Future Interventions.Biomedicines · 2025Review
- Role of branched chain amino acid metabolism on aging.Biogerontology · 2025Review
- The regulatory role of exercise in heart failure and myocardial energy metabolism: A review.Biomolecules & biomedicine · 2025Review
- Plasma metabolomics identifies signatures that distinguish heart failure with reduced and preserved ejection fraction.ESC heart failure · 2025Article
- Athlete's Heart Revisited: Historical, Clinical, and Molecular Perspectives.Circulation research · 2025Review
- α‑ketoglutarate protects against septic cardiomyopathy by improving mitochondrial mitophagy and fission.Molecular medicine reports · 2025Article
- Evidence of Hyperacetylation of Mitochondrial Regulatory Proteins in Left Ventricular Myocardium of Dogs with Chronic Heart Failure.International journal of molecular sciences · 2025Article
130 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAn unbiased systems approach was used to define energy metabolic events that occur during the pathological cardiac remodeling en route to heart failure (HF). METHODS AND
resultsCombined myocardial transcriptomic and metabolomic profiling were conducted in a well-defined mouse model of HF that allows comparative assessment of compensated and decompensated (HF) forms of cardiac hypertrophy because of pressure overload. The pressure overload data sets were also compared with the myocardial transcriptome and metabolome for an adaptive (physiological) form of cardiac hypertrophy because of endurance exercise training. Comparative analysis of the data sets led to the following conclusions: (1) expression of most genes involved in mitochondrial energy transduction were not significantly changed in the hypertrophied or failing heart, with the notable exception of a progressive downregulation of transcripts encoding proteins and enzymes involved in myocyte fatty acid transport and oxidation during the development of HF; (2) tissue metabolite profiles were more broadly regulated than corresponding metabolic gene regulatory changes, suggesting significant regulation at the post-transcriptional level; (3) metabolomic signatures distinguished pathological and physiological forms of cardiac hypertrophy and served as robust markers for the onset of HF; and (4) the pattern of metabolite derangements in the failing heart suggests bottlenecks of carbon substrate flux into the Krebs cycle.
conclusionsMitochondrial energy metabolic derangements that occur during the early development of pressure overload-induced HF involve both transcriptional and post-transcriptional events. A subset of the myocardial metabolomic profile robustly distinguished pathological and physiological cardiac remodeling.
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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.