This study investigates circulating musclin as a biomarker connecting skeletal muscle function and subclinical cardiac dysfunction in patients with cancer, pointing to a shared pathway between cancer-associated muscle wasting and early cardiac impairment.
To the publication →This study examines how acute coronary syndrome impacts long-term survival in cancer patients, providing important prognostic data for this vulnerable patient population.
To the publication →This paper investigates the prevalence of coronary artery disease in patients with an underlying oncological disease and elevated troponin. A key finding is that around 10% of asymptomatic patients with elevated troponin-T had coronary artery disease requiring intervention; classic risk factors such as smoking, elevated BMI and pre-existing coronary artery disease emerged as predictive markers.
To the publication →This observational study characterizes the cardiotoxic effects of BRAF/MEK inhibitor therapy in melanoma patients, contributing real-world safety data for this widely used targeted-therapy combination.
To the publication →In this editorial, we are defining transient cardiomyopathy induced by tyrosine kinase inhibitor therapy as a distinct clinical syndrome in cardio-oncology, calling for standardized diagnostic criteria and management approaches.
To the publication →This publication represents a pivotal step in advancing cardio-oncology by identifying and validating cardio-muscular biomarkers that allow the diagnosis and risk stratification of Immune Checkpoint Inhibitor (ICI)-associated myocarditis. Through integration of large-scale registry analysis, the study moves beyond conventional cardiac markers, introducing cut-offs for clinical decision making. It establishes a benchmark for biomarker-driven management of ICI myocarditis and sets a visionary precedent for personalized, immune-toxicology-guided cardiology.
To the publication →This study sheds new light on the epigenetic control of cardiac gene expression by demonstrating how loss of HDAC4 disrupts global transcriptional repression through H3K9 methylation. Using a cardiomyocyte-specific knockout model, we show that HDAC4 deletion leads to heightened transcriptional responsiveness, revealing a critical buffering role for HDACs in maintaining genomic stability. It shows how epigenetic changes precede transcriptional changes and opens a route for early identification of disease phenotypes.
To the publication →This publication presents the first transcriptomic analysis of myocardial biopsies from patients with immune checkpoint inhibitor (ICI)-associated myocarditis. The study identifies Guanylate Binding Protein 5 (GBP5) as significantly dysregulated, suggesting its involvement in cardiac inflammatory responses. The integration of human biopsy data into cardio-immunology research underscores the potential of tissue-level transcriptomics to refine biomarker discovery and pathophysiological understanding.
To the publication →This study uncovers a previously unrecognized epigenetic-metabolic signaling axis in the heart, linking a proteolytic fragment of HDAC4 to regulation of the hexosamine biosynthetic pathway. The findings demonstrate how neurohumoral stress can induce lasting metabolic reprogramming via chromatin-linked mechanisms. This work has opened new avenues for targeting metabolic remodeling in heart failure and has influenced subsequent research on cardiac epigenetics.
To the publication →This landmark study uncovered a previously unrecognized neurohumoral feedback loop in heart failure by showing that endothelin A receptors on sympathetic neurons impair norepinephrine reuptake, thereby exacerbating cardiac stress. By bridging neurobiology and cardiology, it proposes the peripheral nervous system as a therapeutic target in heart failure and initiated novel strategies to modulate sympathetic outflow in chronic cardiac disease.
To the publication →ABHD5 and partial HDAC4 fragments and variants as a therapeutic approach for the treatment of cardiovascular diseases (#9914912, United States Patent and Trademark Office). This approach targets cardiovascular diseases by employing ABHD5 and specific HDAC4 fragments or variants to modulate cardiac gene expression and remodeling, aiming to reduce maladaptive cardiac hypertrophy and fibrosis.
In vitro method for cardiovascular risk stratification (#14704321.0, European Patent Office). This patent describes an in vitro method for cardiovascular risk stratification, enabling precise prediction of individual patient risk profiles. By analysing specific biomarkers or genetic signatures from patient samples, this diagnostic tool supports personalized treatment decisions and optimized monitoring.
