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Aquisition was done in dda mode with dynamic exclusion."],"repository":["Pride"],"modification":[""],"quantification_method":[""],"data_protocol":["Raw MS data were processed with MaxQuant software (1.6.0.1) 6 with the Andromeda search engine and spectra were matched to a mus musculus-database (17,040 reviewed entries, downloaded from uniprot.org march 2020), a contaminant, and decoy database. A false discovery rate of 0.01 for proteins and peptides, a minimum peptide length of seven amino acids, a mass tolerance of 10 ppm for precursor, and 20 ppm for fragment ions were required. A maximum of two missed cleavages was allowed for the tryptic digest. Cysteine carbamidomethylation was set as a fixed modification, while deamidation (NQ)  and  oxidation (M) were set as variable modifications."],"omics_type":["Proteomics"],"labhead":["Nicolaus Berndt"],"instrument_platform":[""],"submission_type":["PARTIAL"],"labhead_affiliation":["Deutsches Herzzentrum der Charité (DHZC), Institute of Computer-assisted Cardiovascular Medicine"],"species":["Mus Musculus (mouse)"],"publication":["41387378 Ott C, Baumgarten P, Henning T, Weber D, Wallach I, Grune J, Kintscher U, Holzhütter HG, Grune T, Berndt N. Comparative analysis of metabolic and functional cardiac alterations in diet- and genetically induced mouse models of cardiac dysfunction. FEBS J. 2026 293(8):2454-2477 10.1111/febs.70362"],"submitter_mail":["christoph.gille@charite.de"],"submitter_affiliation":["Core  Facility -High-Throughput  Mass  Spectrometry,  Charité"],"submitter_country":["Germany"],"pubmed_abstract":["Cardiac metabolism is highly adaptive, and distinct maladaptive remodeling processes may contribute to the development of cardiac dysfunction. Here, we compared the metabolic, structural, and functional adaptations of two murine models: C57BL/6J mice fed a high-fat, carbohydrate-free diet and New Zealand Obese mice maintained on a standard diet. Cardiac function was assessed by echocardiography, plasma metabolite profiles were analyzed, and cardiac proteomes were quantified by mass spectrometry. Proteomic data were computationally integrated into a kinetic model of cardiac central metabolism (CARDIOKIN1) to predict changes in substrate utilization and ATP production capacities under physiological nutrient conditions. Diet-induced metabolic stress led to cardiac dysfunction with preserved ejection fraction, characterized by mitochondrial dysfunction, impaired ATP production, inflammation, and reduced cardiac mass. Conversely, genetically induced obesity resulted in cardiac impairment with reduced ejection fraction associated with mild fibrosis, maintained ATP production, and substrate switching favoring fatty acid utilization. Proteomic and computational analyses revealed a coordinated downregulation of metabolic networks involved in oxidative phosphorylation, substrate transport, and energy production in both models, but with distinct profiles of metabolic inflexibility and mitochondrial efficiency. This study provides insights of how dietary versus genetic metabolic stress reprograms cardiac metabolism and structure, offering mechanistic insights into the diverse pathways leading to cardiac dysfunction. These insights may guide future strategies for metabolic intervention in heart failure subtypes."],"pubmed_title":["Comparative analysis of metabolic and functional cardiac alterations in diet- and genetically induced mouse models of cardiac dysfunction."],"pubmed_authors":["Ott Christiane C, Baumgarten Patricia P, Henning Thorsten T, Weber Daniela D, Wallach Iwona I, Grune Jana J, Kintscher Ulrich U, Holzhütter Hermann-Georg HG, Grune Tilman T, Berndt Nikolaus N"],"additional_accession":[]},"is_claimable":false,"name":"Comparative analysis of metabolic and functional cardiac alterations in diet- and genetically induced mouse models of heart failure","description":"This study aimed to elucidate the metabolic and functional alterations in heart failure in two mouse models with different heart failure phenotypes. C57BL/6J mice fed a high-fat diet (Black6 HF) and New Zealand Obese mice fed a standard diet (NZO SD) were analyzed compared to Black6 SD controls. Functional parameters of the heart were assessed through echocardiography. Additionally, plasma metabolites and tissue fibrosis were analyzed. Proteomics data from heart tissue were incorporated into a detailed kinetic model of central cardiac metabolism (CARDIOKIN1) to evaluate metabolic capacities. We demonstrate distinct structural and functional cardiac impairments, nutritional imbalances, and metabolic adaptations. Black6 HF mice exhibited cardiac dysfunction with normal ejection fraction, and decreased cardiac mass and inflammation, but without fibrosis while maintaining stable plasma nutrient composition. In contrast, NZO SD mice displayed heart failure with reduced ejection fraction, increased heart mass, significant derangement of circulating plasma nutrients, and mild fibrosis, but no inflammation. Proteomic analysis and kinetic modeling revealed that mitochondrial dysfunction and reduced ATP production capacity are key drivers of heart failure in Black6 HF mice, while NZO SD mice maintained ATP production capacity but showed significant alterations in substrate utilization capacities under variable energy demands. Our findings highlight the critical role of metabolic adaptation in heart failure emphasizing the importance of metabolic flexibility and efficiency. This study underscores the complex interplay between metabolic, structural, and functional changes in heart failure, providing valuable insights into and underpinning the different basis for treatment strategies for different forms of this 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