Targeting Mitochondria-Inflammation Circuit by β-Hydroxybutyrate Mitigates HFpEF

Empagliflozin Blunts Worsening Cardiac Dysfunction Associated With Reduced NLRP3 (Nucleotide-Binding Domain-Like Receptor Protein 3) Inflammasome Activation in Heart Failure

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Extreme Acetylation of the Cardiac Mitochondrial Proteome Does Not Promote Heart Failure

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Nitrosative stress drives heart failure with preserved ejection fraction

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Unlocking the Secrets of Mitochondria in the Cardiovascular System

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Disruption of Acetyl-Lysine Turnover in Muscle Mitochondria Promotes Insulin Resistance and Redox Stress without Overt Respiratory Dysfunction

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Exercise unmasks distinct pathophysiologic features in heart failure with preserved ejection fraction and pulmonary vascular disease

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Mitochondrial dysfunction in pathophysiology of heart failure

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Dapagliflozin and Cardiovascular Outcomes in Type 2 Diabetes

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Interleukin 37 reverses the metabolic cost of inflammation, increases oxidative respiration, and improves exercise tolerance

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Cardiovascular Outcomes and Risks After Initiation of a Sodium Glucose Cotransporter 2 Inhibitor

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Nutritional Ketosis Alters Fuel Preference and Thereby Endurance Performance in Athletes

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Normalization of NAD+Redox Balance as a Therapy for Heart FailureClinical Perspective

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Evidence for Intramyocardial Disruption of Lipid Metabolism and Increased Myocardial Ketone Utilization in Advanced Human Heart Failure

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The Failing Heart Relies on Ketone Bodies as a Fuel

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Phenotype-Specific Treatment of Heart Failure With Preserved Ejection Fraction

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The Emerging Role of Metabolomics in the Diagnosis and Prognosis of Cardiovascular Disease

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A branched-chain amino acid metabolite drives vascular fatty acid transport and causes insulin resistance

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The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease

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Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes

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Metabolomic Fingerprint of Heart Failure with Preserved Ejection Fraction

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Heart Failure With Preserved Ejection Fraction

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Elimination of NADPH Oxidase Activity Promotes Reductive Stress and Sensitizes the Heart to Ischemic Injury

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Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome

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Suppression of Oxidative Stress by  -Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor

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Measurement of cardiac function using pressure–volume conductance catheter technique in mice and rats

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