ReviewNature reviews. Cardiology2025
Cardiac intermediary metabolism in heart failure: substrate use, signalling roles and therapeutic targets.
Review in Nature reviews. Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed.
- In the era of AI, omics and organoids, animal models are still needed in cardiovascular research.Nature reviews. Cardiology · 2026Article
- Xinmailong Injection Attenuates Doxorubicin-Induced Chronic Heart Failure by Regulating the SIRT1/Caspase-3 Axis and Metabolic Reprogramming: An Integrative Network Pharmacology and Metabolomics Study.Current medical science · 2026Article
- Mitochondrial Quality Control in Inherited Mitochondrial Cardiomyopathy: Convergent Pathobiology and a Testable Therapeutic Framework.International journal of molecular sciences · 2026Review
- Discovery of organelle-targeted active ingredients combination from Qifu decoction to treat heart failure via modulating cardiac mitochondria-lysosome dysfunction and contacts.Journal of pharmaceutical analysis · 2026Article
- BCKDK protects against obesity-induced cardiac remodelling and dysfunction by alleviating mitochondrial oxidative stress and ROS-driven MAPK signalling.Redox biology · 2026Article
- Dual SGLT1/2 inhibition with sotagliflozin improves cardiac function and metabolism in type 2 diabetic mice.npj metabolic health and disease · 2026Article
- Pathological Mechanisms and Therapeutic Potential of Mitochondrial Dysfunction in Heart Failure.Reviews in cardiovascular medicine · 2026Review
- A bibliometric analysis of artificial intelligence applications in heart failure.Journal of thoracic disease · 2026Article
- Diet-Associated Regulation of Cardiac Metabolism: Molecular Determinants and Pathophysiological Consequences.Nutrients · 2026Review
- Sirtuins at the Interface of Glucose Metabolism, Diabetes, and Heart Failure: Metabolic Sensing in Cardiometabolic Disease.International journal of molecular sciences · 2026Review
- AMPK Signalling in Heart Failure: From Metabolic Sensor to Context-Dependent Therapeutic Target.Biomedicines · 2026Review
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- High-performance hydrogels in orthopedics: Structural design, performance tuning, and clinical potential.Materials today. Bio · 2026Review
- Molecular Mechanisms and Multi-Omics Integration in Heart Failure: From Pathophysiology to Precision Medicine.International journal of molecular sciences · 2026Review
- Septic Cardiac Remodeling: A New Concept in Cardiac Dysfunction Induced by Experimental Sepsis.Antioxidants (Basel, Switzerland) · 2026Article
- Stretchable large-area transparent nanowire composite arrays for label-free multimodal interrogation of cardiac physiology.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- TIGAR deficiency enhances cardiac resilience through epigenetic programming of Parkin expression.JCI insight · 2026Article
- Defects in auxiliary fuel oxidation and mitochondrial pyruvate transport mark transition to overt heart failure in Tgαq*44 mice.Journal of translational medicine · 2026Article
- Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026Review
- Biomarkers of Cardiac Metabolic Flexibility in Health, HFrEF and HFpEF.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
The number of patients with heart failure is expected to rise sharply owing to ageing populations, poor dietary habits, unhealthy lifestyles and improved survival rates from conditions such as hypertension and myocardial infarction. Heart failure is classified into two main types: heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). These forms fundamentally differ, especially in how metabolism is regulated, but they also have shared features such as mitochondrial dysfunction. HFrEF is typically driven by neuroendocrine activation and mechanical strain, which demands a higher ATP production to sustain cardiac contraction. However, the primary energy source in a healthy heart (fatty acid β-oxidation) is often suppressed in HFrEF. Although glucose uptake increases in HFrEF, mitochondrial dysfunction disrupts glucose oxidation, and glycolysis and ketone oxidation only partially compensate for this imbalance. Conversely, HFpEF, particularly in individuals with metabolic diseases, such as obesity or type 2 diabetes mellitus, results from both mechanical and metabolic overload. Elevated glucose and lipid levels overwhelm normal metabolic pathways, leading to an accumulation of harmful metabolic byproducts that impair mitochondrial and cellular function. In this Review, we explore how disruptions in cardiac metabolism are not only markers of heart failure but also key drivers of disease progression. We also examine how metabolic intermediates influence signalling pathways that modify proteins and regulate gene expression in the heart. The growing recognition of the role of metabolic alterations in heart failure has led to groundbreaking treatments that target these metabolic disruptions, offering new hope for these patients.
Indexed as
Identifiers
40544173What 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.