ArticleCommunications medicine2025
Modulation of cardiac fatty acid or glucose oxidation to treat heart failure in preclinical models: a systematic review and meta-analysis.
Article in Communications medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed.
- Treatment with the Nox1/4 inhibitor Setanaxib ameliorates cardiac function in mouse models of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Innovative Advances in Non-Invasive Detection Technologies for Heart Failure: Synergistic Application of Multimodal Sensing and Intelligent Algorithms.Reviews in cardiovascular medicine · 2026Review
- A comprehensive review of ischemic heart disease: pathophysiology, current treatments, natural products-based therapies, and nanotherapeutics.Frontiers in pharmacology · 2026Review
- Metabolic regulation for the treatment of ischemic heart disease with stem cells and extracellular vesicles.NPJ cardiovascular health · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCurrent expert opinion on cardiac metabolism in heart failure (HF) suggests that inhibiting cardiac fatty acid oxidation (FAO) or stimulating cardiac glucose oxidation (GO) can improve heart function. However, systematic evidence is lacking, and contradictory data exist. Therefore, we conducted a comprehensive meta-analysis to assess the effects of modulating myocardial GO or FAO on heart function.
methodsWe screened MEDLINE via Ovid, Scopus, and Web of Science until March 02, 2024 for interventional studies reporting significant changes in cardiac GO or FAO in established animal models of HF, such as ischemia-reperfusion, pressure overload, rapid pacing, and diabetic cardiomyopathy. We employed multivariate analysis (four-level random-effects model) to enclose all measures of heart function. Additionally, we used meta-regression to explore heterogeneity and contour-enhanced funnel plots to assess publication bias. The protocol is registered on PROSPERO (CRD42023456359).
resultsOf a total of 10,628 studies screened, 103 studies are included. Multivariate meta-analysis reveals that enhancing cardiac GO considerably restores cardiac function (Hedges' g = 1.03; 95% CI: 0.79-1.26; p < 0.001). Interestingly, interventions associated with reduced myocardial FAO show neutral effects (Hedges' g = 0.24; 95% CI: -0.57-1.05; p = 0.557), while those augmenting myocardial FAO markedly improve function (Hedges' g = 1.17; 95% CI: 0.58-1.76; p < 0.001).
conclusionsOur data underscore the role of cardiac metabolism in treating HF. Specifically, these results suggest that stimulating either myocardial FAO or GO may considerably improve cardiac function. Furthermore, these results question the current notion that inhibition of cardiac FAO is protective.
Identifiers
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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.