ReviewThe Journal of physiology2004
Energy metabolism in heart failure.
Review in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04105803 (Cardiac Mitochondrial Function After Heart Transplantation), which is not on this map. Cited by 210 papers, 1 of them a synthesis 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.
Cardiac Mitochondrial Function After Heart Transplantation
Who cites it
210 citing papers in PubMed, 1 synthesis or guideline pooled it, 509 citations in OpenAlex.
- Recent Developments in the Role of Coenzyme Q10 for Coronary Heart Disease: a Systematic Review.Current atherosclerosis reports · 2018Pooled it
- A comprehensive assessment of carbon monoxide caused mortality via bioinformatics assisted untargeted metabolomics analysis.Forensic science, medicine, and pathology · 2026Article
- Pathogenic role of mitochondrial DNA mutations in heart failure: clinical features, mechanisms, and therapeutic prospects.Frontiers in cardiovascular medicine · 2026Review
- Dynamic proteome profiling of differentiating human embryonic stem cells towards cardiomyocytes.Scientific reports · 2025Article
- Drug Repositioning in Doxorubicin-Induced Cardiotoxicity Protection.International journal of molecular sciences · 2025Review
- Oxidative Stress, Mitochondrial Quality Control, Autophagy, and Sirtuins in Heart Failure.International journal of molecular sciences · 2025Review
- DDX3X/MAVS alleviates doxorubicin‑induced cardiotoxicity by regulating stress granules.Molecular medicine reports · 2025Article
- Dietary influences on chemotherapy sensitivity and cardiotoxicity modulated by IRE1 targeting in triple-negative breast cancer in female mice.Physiological reports · 2025Article
- The triglyceride glucose (TyG) index is associated with decreased myocardial mechano-energetic efficiency in individuals with different glucose tolerance status.European journal of clinical investigation · 2025Article
- Role of Gut Microbial Metabolites in Ischemic and Non-Ischemic Heart Failure.International journal of molecular sciences · 2025Review
- Acetylation in Cardiac Aging: Molecular Mechanism and Therapeutic Approaches.Results and problems in cell differentiation · 2025Review
- Evolution of Theories on Doxorubicin-Induced Late Cardiotoxicity-Role of Topoisomerase.International journal of molecular sciences · 2024Review
- The Wilms' Tumor Suppressor WT1 in Cardiomyocytes: Implications for Cardiac Homeostasis and Repair.Cells · 2024Review
- Advances in myocardial energy metabolism: metabolic remodelling in heart failure and beyond.Cardiovascular research · 2024Review
- 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens.Antioxidants (Basel, Switzerland) · 2024Article
- The treatment of chronic anemia in heart failure: a global approach.Clinical research in cardiology : official journal of the German Cardiac Society · 2024Review
- Insulin-Heart Axis: Bridging Physiology to Insulin Resistance.International journal of molecular sciences · 2024Review
- Mitochondrial dysfunction is associated with hypertrophic cardiomyopathy in Pompe disease-specific induced pluripotent stem cell-derived cardiomyocytes.Cell proliferation · 2024Article
- Growing concerns about using hypoxia-inducible factor prolyl hydroxylase inhibitors for the treatment of renal anemia.Clinical kidney journal · 2024Review
- Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2024Review
150 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a syndrome resulting from the inability of the cardiac pump to meet the energy requirements of the body. Despite intensive work, the pathogenesis of the cardiac intracellular abnormalities that result from HF remains incompletely understood. Factors that lead to abnormal contraction and relaxation in the failing heart include metabolic pathway abnormalities that result in decreased energy production, energy transfer and energy utilization. Heart failure also affects the periphery. Patients suffering from heart failure always complain of early muscular fatigue and exercise intolerance. This is linked in part to intrinsic alterations of skeletal muscle, among which decreases in the mitochondrial ATP production and in the transfer of energy through the phosphotransfer kinases play an important role. Alterations in energy metabolism that affect both cardiac and skeletal muscles argue for a generalized metabolic myopathy in heart failure. Recent evidence shows that decreased expression of mitochondrial transcription factors and mitochondrial proteins are involved in mechanisms causing the energy starvation in heart failure. This review will focus on energy metabolism alterations in long-term chronic heart failure with only a few references to compensated hypertrophy when necessary. It will briefly describe the energy metabolism of normal heart and skeletal muscles and their alterations in chronic heart failure. It is beyond the scope of this review to address the metabolic switches occurring in compensated hypertrophy; readers could refer to well-documented reviews on this subject.
Indexed as
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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.