bims-hafaim Biomed News
on Heart failure metabolism
Issue of 2026–06–14
seven papers selected by
Kyle McCommis, Saint Louis University



  1. Clin Sci (Lond). 2026 Jun 10. pii: CS20261501. [Epub ahead of print]
      Cardiometabolic heart failure with preserved ejection fraction (HFpEF) is a heterogenous metabolic disease, which in the heart presents as left ventricle diastolic dysfunction, ventricular stiffness, and myocardial structural remodeling. Deleterious changes in cardiac metabolism are central to HFpEF pathophysiology, and proposed treatments for the disease have focused on repairing these defects. In this study, we used a preclinical mouse model that recapitulates cardiometabolic HFpEF to elucidate the molecular mechanisms driving cardiac dysfunction, and tested whether recombinant adropin (a liver- and brain-derived endogenous peptide hormone) could reverse observed defects. We show that long-term treatment with adropin reversed multiple markers of HFpEF-related cardiac dysfunction (including fibrosis, diastolic dysfunction, and cardiomyocyte hypertrophy). Using untargeted metabolomics, we found that adropin treatment reduced hexosamine biosynthesis pathway activity, leading to a reduction in the O-GlcNAcylation of the cardiac fatty acid oxidation enzyme long chain acyl-CoA dehydrogenase (LCAD). Reducing LCAD O-GlcNAcylation increased LCAD activity in vitro, and reduced the accumulation of long-chain acylcarnitines in HFpEF mouse hearts in vivo. Our results suggest that adropin may restore cardiac metabolic function in HFpEF, and that targeting this pathway may be a novel therapeutic avenue for this disease.
    Keywords:  fatty acid oxidation; heart failure; mitochondria
    DOI:  https://doi.org/10.1042/CS20261501
  2. J Mol Cell Cardiol. 2026 Jun 05. pii: S0022-2828(26)00089-1. [Epub ahead of print]
       BACKGROUND AND HYPOTHESIS: Hypertrophic cardiomyopathy (HCM) is considered a metabolic disease, but it is unknown whether all sarcomeric protein gene mutations lead to similar derangements of cardiac energy metabolism. Our prior studies showing differences in mitochondrial function in mouse models led us to hypothesize that HCM mutations lead to allele-specific metabolic pathway remodeling. In order to test this hypothesis, we examined cardiac substrate utilization using a triple tracer approach that simultaneously assays fatty acid (FA), ketone, and glucose oxidation, in R403Q-MyHC and R92W-TnT perfused hearts at established disease stage.
    METHODS: Mouse hearts (14-16 weeks old) were Langendorff-perfused to steady state 13C enrichment (~30 min) while placed in a 14.1 T NMR for in situ 31P spectroscopy. The perfusate contained substrates which each produce distinctively labeled acetyl-CoA: [1,6-13C2]glucose, [U13C]mixed fatty acids, and [1,3-13C2]β-hydroxybutyrate. At the end of perfusion, hearts were freeze clamped and extracted for 13C NMR isotopomer analysis. Oxygen concentration in afferent/efferent perfusate was measured using a Clark electrode, and used to compute myocardial oxygen consumption rate (MVO2).
    RESULTS: Using a model of citric acid cycle (CAC) metabolism that equates MVO2 with production of reducing equivalents, we observed significantly lower fatty acid (FA) oxidation and pyruvate dehydrogenase (PDH) flux in MyHC mutants, but similar substrate utilization in TnT mutants, when compared to respective controls. 31P-spectroscopy revealed significantly lower energy reserves reflected by lower PCr/ATP ratios in MyHC mutants, but similar PCr/ATP ratios in TnT mutants compared to controls.
    CONCLUSION: Cardiac metabolic flux measurements revealed an energy-deficient cardiac phenotype in R403Q-MyHC mutants, but not R92W-TnT mutants, reflecting allele-specific remodeling of cardiac energy metabolism. These results suggest that therapeutics aimed at downregulation of FA or carbohydrate metabolism may have mutation-specific effects.
    Keywords:  (13)C NMR; HCM; Metabolic flux; MyHC; TnT
    DOI:  https://doi.org/10.1016/j.yjmcc.2026.06.005
  3. J Am Heart Assoc. 2026 Jun 09. e048427
       BACKGROUND: Heart failure with ischemic cause is associated with substantial cardiovascular mortality. SGLT2 (sodium glucose cotransporter 2) inhibitors demonstrate cardiovascular benefits, but interindividual response variability remains poorly understood. We investigated the relationship between baseline ketone body metabolism and SGLT2 inhibitor response in heart failure with ischemic cause across diverse genetic backgrounds.
    METHODS: We analyzed metabolomics data from 3847 patients with heart failure with ischemic cause across 23 countries (2020-2024). Ketone body metabolites (β-hydroxybutyrate, acetoacetate, acetone) were quantified by liquid chromatography-mass spectrometry. SGLT2 inhibitor response was assessed via a composite end point including cardiovascular mortality, heart failure hospitalization, and kidney function decline. Analyses included multivariate Cox regression, machine learning (Random Forest, Extreme Gradient Boosting), and Mendelian randomization, integrating Global Burden of Disease 2021 data across 5 genetic ancestry groups.
    RESULTS: Baseline β-hydroxybutyrate inversely correlated with SGLT2 inhibitor outcomes (r=-0.67, P<0.001). The lowest ketone tertile demonstrated superior outcomes (hazard ratio [HR], 0.58 [95% CI, 0.51-0.66], P<0.001), and the highest tertile showed elevated risk (HR, 1.58 [95% CI, 1.39-1.79], P<0.001). East Asian populations exhibited 34.24% higher baseline ketone levels (2.47±0.83 versus 1.84±0.61 mmol/L, P<0.001) with attenuated treatment benefit versus European ancestry. Machine learning models achieved area under the receiver operating characteristic curve of 0.8245 (95% CI, 0.8012-0.8478) predicting individual outcomes from baseline metabolomic profiles.
    CONCLUSIONS: Baseline ketone body metabolism is strongly associated with SGLT2 inhibitor outcomes in heart failure with ischemic cause, with marked interancestry variability. Metabolomic profiling may inform precision medicine approaches to therapeutic decision-making, pending prospective validation.
    Keywords:  Global Burden of Disease; SGLT2 inhibitors; genetic diversity; heart failure; ischemic heart disease; ketone bodies; metabolomics
    DOI:  https://doi.org/10.1161/JAHA.125.048427
  4. bioRxiv. 2026 Jun 02. pii: 2026.05.29.728910. [Epub ahead of print]
       Background: Impaired myocardial metabolism is a defining feature of heart failure, but many defective pathways and mechanisms remain to be identified. Prior studies find phosphoglycerate kinase and its synthesized product 3-phospho-glycerate required for the serine synthetic pathway (SSP) are reduced in human HFpEF myocardium. As serine is also provided exogenously, the impact of SSP reduction is uncertain. Here, we tested if and how SSP decline coupled to phosphoglycerate dehydrogenase (PHGDH) impacts cardiomyocyte (CM) and whole heart metabolic remodeling and stress responses.
    Methods: Studies were performed in isolated CMs and mice with CM-selective knock-down of PHGDH. Using pharmacological inhibition or genetic silencing of PHGDH, we tested their impact on CM one-carbon metabolism pathways, cell hypertrophic responses, mitochondrial respiration, and in vivo functional, structural, and metabolic adaptations to pressure-overload stress.
    Results: In CMs, PHGDH inhibition caused dose-dependent serine depletion linearly coupled with cytotoxicity, accompanied by NAD/NADH and GSH/GSSG imbalance, reduced ATP, and disruption of one-carbon and nucleotide metabolites. Stable-isotope tracing revealed distinct metabolic fates of glucose-derived (SSP) versus exogenous serine. Exogenous serine did not rescue PHGDH-deficient CMs, whereas combined ribose and an anti-oxidant (DTT) attenuated injury and reduced nucleotide pools. PHGDH suppression reduced amino acid abundance, impaired nascent protein synthesis, and blunted endothelin-1-induced hypertrophic and mitochondrial respiration. In vivo , cardiomyocyte-specific PHGDH heterozygous mice (PHGDH +/- ) had no basal phenotype, but amplified chamber dilation, dysfunction, fibrosis, and mortality 4 weeks after transverse aortic constriction (TAC). Corresponding increases in amino acids, one-carbon metabolites, nucleotides, and TCA-cycle intermediates in wild-type TAC hearts were significantly blunted in PHGDH +/- hearts.
    Conclusions: Cardiomyocyte SSP is a critical regulator of redox balance, one-carbon metabolism, purine synthesis, amino acid homeostasis, and growth-related pathways required for cardiac adaptation to pressure overload. It is non-redundant with exogenous serine by providing distinct influences on key metabolic pathways and is a potential therapeutic target.
    DOI:  https://doi.org/10.64898/2026.05.29.728910
  5. World J Crit Care Med. 2026 Jun 09. 15(2): 117717
       BACKGROUND: Ketone bodies, especially β-hydroxybutyrate, have shown the potential to improve hemodynamic outcomes such as cardiac output (CO) and left ventricular ejection fraction (LVEF) in patients with heart failure (HF). However, the overall effectiveness of ketone body supplementation in this population remains uncertain. Therefore, we conducted this systematic review and meta-analysis to evaluate the impact of ketone body supplementation on cardiac and hemodynamic parameters in patients with HF while accounting for the limited and emerging nature of the available randomized evidence.
    AIM: To evaluate the impact of ketone body supplementation on cardiac and hemodynamic parameters in patients with HF while accounting for the limited and emerging nature of the available randomized evidence.
    METHODS: A systematic search of PubMed, Scopus, EMBASE, and the Cochrane Central Register of Controlled Trials was conducted from inception to March 2025, with additional screening of ClinicalTrials.gov for unpublished or ongoing trials. Randomized controlled trials (RCTs) comparing ketone body supplementation with placebo in patients with HF were included. Statistical analyses were performed using a random-effects model in RevMan 5.4 to calculate weighted mean differences (MDs) with 95% confidence intervals (CIs). Outcomes assessed included CO, systemic vascular resistance, LVEF, heart rate, venous oxygen saturation, pulmonary capillary wedge pressure, and other cardiac functional indices. Given the small number of included studies, subgroup analyses were considered exploratory.
    RESULTS: Four randomized controlled trials involving a total of 94 patients were included. Compared with placebo, ketone supplementation was associated with a significant increase in CO (MD = 1.11, 95%CI: 0.13-2.09, P = 0.03) and a reduction in systemic vascular resistance (MD = -252.61, 95%CI: -475.72 to -29.50, P = 0.03). Improvements were also observed in LVEF (MD = 3.31, 95%CI: 0.39-6.22, P = 0.03), venous oxygen saturation (MD = 3.33, 95%CI: -0.01 to 6.68, P = 0.05), and pulmonary capillary wedge pressure (MD = -1.09, 95%CI: -1.60 to -0.59, P < 0.0001), along with an increase in heart rate (MD = 4.08, 95%CI: 3.00-5.17, P < 0.0001). Subgroup analyses by HF phenotype (HF with reduced ejection fraction vs HF with preserved ejection fraction) suggested differential effects; however, several subgroups included only one study and should be interpreted as hypothesis-generating only. No statistically significant changes were observed in global longitudinal strain, left ventricular end-diastolic volume, or tricuspid annular plane systolic excursion, and substantial heterogeneity and potential small-study effects limit the robustness of pooled estimates.
    CONCLUSION: Ketone body supplementation was associated with short-term improvements in selected hemodynamic and cardiac functional parameters in patients with HF. However, these findings are based on a small number of short-duration trials with limited sample sizes and crossover designs, precluding firm clinical conclusions. Larger, well-powered randomized trials with longer follow-up are required to confirm the therapeutic role, optimal dosing, and clinical impact of ketone supplementation in HF.
    Keywords:  3-β-hydroxybutyrate; Cardiac output; Heart failure; Ketone bodies; Left ventricular ejection fraction
    DOI:  https://doi.org/10.5492/wjccm.v15.i2.117717
  6. Nutrients. 2026 May 25. pii: 1688. [Epub ahead of print]18(11):
      Heart failure (HF) remains associated with high morbidity and mortality, with heart failure with preserved ejection fraction (HFpEF) becoming increasingly prevalent and therapeutically challenging despite advances in pharmacological and rehabilitative care. Beyond their glucose-lowering effects, glucagon-like peptide-1 receptor agonists (GLP-1RAs) confer cardiometabolic benefits and may serve as effective adjuncts to cardiac rehabilitation (CR), particularly in obese patients with HFpEF. Obesity plays a central role in the pathophysiology of HFpEF, and GLP-1RAs promote weight loss, reduce insulin resistance and leptin signaling, and improve hemodynamic and metabolic abnormalities associated with HFpEF. Accumulating evidence suggests that the benefits of GLP-1RAs are phenotype-specific and more pronounced in patients with HFpEF than in patients with HF with reduced ejection fraction. Current clinical guidelines recommend GLP-1RAs for patients who have type 2 diabetes mellitus and established cardiovascular (CV) disease or are at high CV risk, with recent updates recognizing their potential benefits in patients with HFpEF and obesity. Cardiac rehabilitation, delivered through multidisciplinary programs, remains a cornerstone of HF management. Although caloric restriction and aerobic exercise can be beneficial in patients with HFpEF and obesity, these interventions alone are often insufficient. Sarcopenia is common in older patients with HFpEF and contributes to adverse outcomes, underscoring the importance of incorporating resistance training into CR programs. The most frequent adverse effects of GLP-1RAs are gastrointestinal events, which are generally mild to moderate but may lead to treatment discontinuation in some patients. Future studies should investigate the potential synergistic effects of GLP-1RAs and CR, clarify their long-term safety and efficacy in HF populations, and define their role beyond obese HFpEF phenotypes.
    Keywords:  GLP-1 receptor agonists; cardiac rehabilitation; heart failure; obesity; sarcopenia
    DOI:  https://doi.org/10.3390/nu18111688
  7. Circ Rep. 2026 Jun 10. 8(6): 891-900
       Background: Exercise-based cardiac rehabilitation is effective for improving the prognosis of patients with heart failure (HF), but little is known about its interactions with dietary components. We investigated the impacts of dietary fat intake and its source on the cardioprotective effects of exercise in mice with HF.
    Methods and Results: Endurance exercise and diets with different fat composition, including a normal diet (NE: 11% fat), a soybean oil-rich diet (SE: 32% fat) and a lard-rich diet (LE: 32% fat), were provided for 4 weeks to mice with HF induced by transverse aortic constriction. Exercise improved left ventricular systolic function and suppressed cardiac hypertrophy in the NE and SE groups, but these effects were attenuated in the LE group. The LE group exhibited a reduction in linoleic acid content within mitochondrial phospholipids such as phosphatidylcholine and phosphatidylethanolamine, concurrent with the promotion of cardiolipin remodeling pathways. This resulted in a marked reduction in tetralinoleoyl cardiolipin (L4CL), which is crucial for maintaining mitochondrial membrane function. This was supported by the finding that assembly of mitochondrial respiratory chain supercomplexes was partially impaired in the LE group.
    Conclusions: Lard intake may attenuate the exercise-induced cardioprotective effects against HF by reducing myocardial L4CL levels and impairing mitochondrial supercomplex assembly involved in mitochondrial respiratory capacity.
    Keywords:  Exercise; Heart failure; High-fat diet; Mitochondrial supercomplex; Tetralinoleoyl cardiolipin
    DOI:  https://doi.org/10.1253/circrep.CR-25-0297