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Metabolic diseases are important risk factors for the development of heart failure, and energetic deficit and oxidative stress are important in its pathophysiology. A Focus issue in Nature Reviews Cardiology appraises the metabolic alterations in heart failure, with an emphasis on substrate and intermediate metabolism, vascular dysfunction, inflammation and mechano-energetic uncoupling, integrating these different pathomechanistic angles into one cohesive view.
Artificial intelligence (AI) technologies are revolutionizing cardiovascular health by analysing environmental factors at an unprecedented scale. Geospatial AI integrates vast datasets — from satellite imagery down to street-level views — to identify complex risk patterns, which enables personalized predictions and guides precision interventions to mitigate the environmental burden of disease.
In this Tools of the Trade article, Rukshan Ahamed Mohamed Rafeek and Natkunam Ketheesan describe the utility of the Lewis rat autoimmune valvulitis model in assessing potential therapeutic applications for rheumatic heart disease.
According to a study published in Nature, the gut microbial metabolite imidazole propionate can induce atherosclerosis in atheroprone mice, further highlighting the role of microbiome-informed precision medicine to treat cardiovascular disease.
Jae Hyun Byun and Stella S. Daskalopoulou describe the study that identified lipoprotein(a) as a genetically determined contributor to coronary artery disease.
In this Review, Mericskay and colleagues discuss the role of cardiac intermediary metabolism in heart failure, describing the perturbations in cardiac energy metabolism that occur in heart failure with reduced ejection fraction and cardiometabolic heart failure with preserved ejection fraction, and highlighting potential treatments to target intermediary metabolism in these patients.
Coronary and systemic vascular dysfunction contributes to the initiation and progression of heart failure (HF) with or without reduced ejection fraction and, vice versa, HF compromises vascular function. In this Review, Liberale and colleagues discuss vascular dysfunction in the pathogenesis of HF and how pharmacological, interventional and surgical management of HF can improve vascular function.
In this Review, the authors discuss the cellular and molecular mechanisms of immunometabolism in heart failure and highlight potential approaches for non-invasive monitoring and for the treatment of patients with heart failure.
In this Review, the authors focus on the tight interaction between cardiac mechanics and mitochondrial energetics, discuss how this mechano-energetic coupling is disturbed in various acquired and inherited forms of heart failure, and summarize the established and emerging treatments for heart failure that target this mechano-energetic uncoupling.
In this Review, Ravindran and Gustafsson describe the mechanisms involved in regulating mitochondrial quality control in cardiomyocytes, discuss how these pathways are altered in cardiovascular disease and ageing, and highlight the therapeutic potential of targeting mitochondrial quality control pathways in cardiovascular disease.
Treatment of cardiomyopathies has historically focused on symptom management. In this Review, Elliott and colleagues discuss how elucidation of the complex cellular and molecular pathways has led to the development of novel therapeutic agents that modify or mitigate the effects of causative genetic variants, enabling tailored treatment for cardiomyopathies.
