ReviewCell metabolism2015
Altered myocardial calcium cycling and energetics in heart failure--a rational approach for disease treatment.
Review in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
136 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- A modified method for isolation of human cardiomyocytes to model cardiac diseases.Journal of translational medicine · 2018Trial
- Cardiac unloading models for myocardial reverse remodeling.Basic research in cardiology · 2026Review
- Evaluating and comparing the signalling and functional landscape of hiPSC-CMs derived from patients with dilated cardiomyopathy.npj biomedical innovations · 2026Article
- Mitochondrial protein OPA3 sustains cardiac function by regulating calcium handling in male mice.Nature communications · 2026Article
- Interplay between variability in intrinsic cellular properties and heart failure-associated remodeling in a simulated population with human heart failure.Journal of molecular and cellular cardiology · 2026Article
- Disruption of ATP Synthase Spatiotemporal Organization, CaAging cell · 2026Article
- Leveraging the shared and opposing genetic mechanisms in the heritable cardiomyopathies.Research square · 2026Article
- Biomarkers of Cardiac Metabolic Flexibility in Health, HFrEF and HFpEF.International journal of molecular sciences · 2026Review
- Adipocyte fatty acid-binding protein 4 suppresses contraction of mouse ventricular myocytes via a calcium-independent pathway.Frontiers in physiology · 2026Article
- Cardiomyocyte-derived OTUD7B promotes cardiac hypertrophy by deubiquitinating SERCA2a.Theranostics · 2026Article
- Aberrant myocardial calcium cycling: pathogenic mechanisms and targeted therapeutics for heart failure.Frontiers in cardiovascular medicine · 2026Review
- Microprotein, macro-effect: DWORF as a therapeutic strategy in heart failure.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial remodeling in heart failure with reduced ejection fraction.Frontiers in physiology · 2026Review
- Molecular insights in HIV-associated cardiac dysfunction.Communications medicine · 2025Article
- Mitochondrial Dysfunction Contributes to Decompensation in a Zebrafish Model of Isoproterenol-Induced Heart Failure.Acta physiologica (Oxford, England) · 2025Article
- A Molecular Perspective on the Intricate Interplay Among Exosomes, Bioenergetic Metabolism, and the Pathogenesis of Diabetic Cardiomyopathy.Journal of cardiovascular translational research · 2025Review
- A circular RNA derived from the ryanodine receptor 2 locus controls cardiac hypertrophy and calcium handling.Cellular and molecular life sciences : CMLS · 2025Article
- From Gut to Heart: Targeting Trimethylamine N-Oxide as a Novel Strategy in Heart Failure Management.Biomolecules · 2025Review
- GLP-1 Receptor Agonists in Heart Failure.Biomolecules · 2025Review
76 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
Abstract
Cardiomyocyte function depends on coordinated movements of calcium into and out of the cell and the proper delivery of ATP to energy-utilizing enzymes. Defects in calcium-handling proteins and abnormal energy metabolism are features of heart failure. Recent discoveries have led to gene-based therapies targeting calcium-transporting or -binding proteins, such as the cardiac sarco(endo)plasmic reticulum calcium ATPase (SERCA2a), leading to improvements in calcium homeostasis and excitation-contraction coupling. Here we review impaired calcium cycling and energetics in heart failure, assessing their roles from both a mutually exclusive and interdependent viewpoint, and discuss therapies that may improve the failing myocardium.
Indexed as
Identifiers
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.