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Showing 1–21 of 21 results
Advanced filters: Author: Christoph Maack Clear advanced filters

  • Diabetes can cause heart failure by a toxic accumulation of lipids in cardiac myocytes, which impairs their function. This work shows that stimulation of the bile acid receptor TGR5 limits fatty acid uptake into cardiac myocytes and prevents the development of diabetic cardiomyopathy.

    • David Weissman
    • Christoph Maack
    News & Views
    Nature Metabolism
    Volume: 6, P: 993-995

  • 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.

    • Christoph Maack
    Comments & Opinion
    Nature Reviews Cardiology
    Volume: 22, P: 695-696

  • Electrical stimulation of the brain can have variable effects, perhaps because of individual differences in brain structure which produce differences in the electric fields. Here, the authors show that using functional and structural brain imaging along with electric field modeling can predict the effectiveness of stimulation.

    • Florian H. Kasten
    • Katharina Duecker
    • Christoph S. Herrmann
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-11

  • The results of EMPATROPISM-FE, a post hoc analysis of the EMPA-TROPISM trial performed by Angermann et al., suggest that the beneficial effects of empagliflozin treatment in heart failure populations may be related to changes in iron metabolism.

    • Christiane E. Angermann
    • Carlos G. Santos-Gallego
    • Juan J. Badimon
    ResearchOpen Access
    Nature Cardiovascular Research
    Volume: 2, P: 1032-1043

  • Reil, Sequeira et al. investigate the role of mechanical dyssynchrony in Takotsubo Syndrome, revealing significant segmental dysfunction in the left ventricle. Their findings highlight the mechanical inefficiencies and reduced systolic function in Takotsubo patients, independent of electrical conduction abnormalities.

    • Jan-Christian Reil
    • Vasco Sequeira
    • Thomas Stiermaier
    ResearchOpen Access
    Communications Medicine
    Volume: 4, P: 1-9

  • Heart failure is a systemic disease in which neuroendocrine activation, inflammation and metabolic changes can impair cardiac function. In addition, variants in genes encoding sarcomeric proteins can predispose individuals to develop heart failure. The 2022 Gordon Research Conference on Cardiac Regulatory Mechanisms aims to identify novel treatment targets by applying high-resolution approaches to complex cardiac disorders.

    • Christoph Maack
    • Jil C. Tardiff
    Comments & Opinion
    Nature Reviews Cardiology
    Volume: 19, P: 343-344

  • In this Review, Maack and colleagues discuss the pathophysiology of angina in the context of the underlying cardiovascular condition as well as the modes of action of antianginal drugs to provide the clinician with a rationale and compass of when to use which compound or combination of drugs.

    • Edoardo Bertero
    • Gerd Heusch
    • Christoph Maack
    Reviews
    Nature Reviews Cardiology
    Volume: 18, P: 838-852

  • In patients with heart failure, derangements of substrate utilization and intermediate metabolism, an energetic deficit, and oxidative stress are thought to underlie contractile dysfunction and disease progression. In this Review, Bertero and Maack describe the physiological processes of cardiac energy metabolism and their pathological alterations in heart failure and diabetes mellitus, and discuss promising treatments targeting substrate utilization or oxidative stress in mitochondria.

    • Edoardo Bertero
    • Christoph Maack
    Reviews
    Nature Reviews Cardiology
    Volume: 15, P: 457-470

  • 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.

    • Dunja Aksentijevic
    • Simon Sedej
    • Christoph Maack
    Reviews
    Nature Reviews Cardiology
    Volume: 22, P: 773-797

  • A proteolytically derived fragment of the epigenetic regulator HDAC4 protects the heart through transcriptional repression of the hexosamine biosynthetic pathway, thereby inhibiting protein O-GlcNAcylation and maintaining normal calcium handling and contractility of cardiomyocytes.

    • Lorenz H Lehmann
    • Zegeye H Jebessa
    • Johannes Backs
    Research
    Nature Medicine
    Volume: 24, P: 62-72

  • Induction of cardiac contractility, although desirable for restoring heart function, often has long-term detrimental effects. From studies on RKIP, an upstream regulator of β-adrenergic receptor signaling, Schmid et al. show that cardiac contractility in mice can be increased in a well-tolerated manner through the balanced activation of the β1 and β2 subtypes of the adrenergic receptor.

    • Evelyn Schmid
    • Stefan Neef
    • Kristina Lorenz
    Research
    Nature Medicine
    Volume: 21, P: 1298-1306

  • 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.

    • Mathias Mericskay
    • Coert J. Zuurbier
    • Gabriele G. Schiattarella
    Reviews
    Nature Reviews Cardiology
    Volume: 22, P: 704-727

  • CNP/cGMP signaling counteracts metabolic reprogramming in pulmonary arterial hypertension pericytes by reducing HIF1α, GLUT-1, and CAD activity, thereby normalizing glycolysis and pyrimidine synthesis and limiting hyperproliferation, highlighting its therapeutic potential.

    • Minhee Noh
    • Ankita Mitra
    • Swati Dabral
    ResearchOpen Access
    Communications Biology
    Volume: 8, P: 1-16