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Open AccessMitochondrial calcium in cardiac ischemia/reperfusion injury and cardioprotection
Mitochondrial calcium (Ca2+) signals play a central role in cardiac homeostasis and disease. In the healthy heart, mitochondrial Ca2+ levels modulate the rate of oxidative metabolism to match the rate of adenosin...
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Article
Bile acids for diabetic cardiomyopathy
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 in...
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Article
Open AccessThe challenges of research data management in cardiovascular science: a DGK and DZHK position paper—executive summary
The sharing and documentation of cardiovascular research data are essential for efficient use and reuse of data, thereby aiding scientific transparency, accelerating the progress of cardiovascular research and...
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Article
Open AccessFabry Disease: Cardiac Implications and Molecular Mechanisms
This review explores the interplay among metabolic dysfunction, oxidative stress, inflammation, and fibrosis in Fabry disease, focusing on their potential implications for cardiac involvement. We aim to discus...
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Open AccessEpigenetic modulators link mitochondrial redox homeostasis to cardiac function in a sex-dependent manner
While excessive production of reactive oxygen species (ROS) is a characteristic hallmark of numerous diseases, clinical approaches that ameliorate oxidative stress have been unsuccessful. Here, utilizing multi...
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Article
Open AccessA new approach to characterize cardiac sodium storage by combining fluorescence photometry and magnetic resonance imaging in small animal research
Cardiac myocyte sodium (Na+) homoeostasis is pivotal in cardiac diseases and heart failure. Intracellular Na+ ([Na+]i) is an important regulator of excitation–contraction coupling and mitochondrial energetics. In...
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Open AccessActivation of the integrated stress response rewires cardiac metabolism in Barth syndrome
Barth Syndrome (BTHS) is an inherited cardiomyopathy caused by defects in the mitochondrial transacylase TAFAZZIN (Taz), required for the synthesis of the phospholipid cardiolipin. BTHS is characterized by heart ...
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Open AccessEmpagliflozin effects on iron metabolism as a possible mechanism for improved clinical outcomes in non-diabetic patients with systolic heart failure
Sodium-glucose co-transporter-2 (SGLT2) inhibitors improve clinical outcomes in patients with heart failure (HF), but mechanisms of action are incompletely understood. In the EMPA-TROPISM trial, empagliflozin ...
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Article
Open AccessAn arrhythmogenic metabolite in atrial fibrillation
Long-chain acyl-carnitines (ACs) are potential arrhythmogenic metabolites. Their role in atrial fibrillation (AF) remains incompletely understood. Using a systems medicine approach, we assessed the contributio...
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Open AccessCardiac Involvement in Mitochondrial Disorders
We review pathophysiology and clinical features of mitochondrial disorders manifesting with cardiomyopathy.
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Open AccessMitochondrial Fission Process 1 controls inner membrane integrity and protects against heart failure
Mitochondria are paramount to the metabolism and survival of cardiomyocytes. Here we show that Mitochondrial Fission Process 1 (MTFP1) is an inner mitochondrial membrane (IMM) protein that is dispensable for m...
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Open AccessTachycardiomyopathy entails a dysfunctional pattern of interrelated mitochondrial functions
Tachycardiomyopathy is characterised by reversible left ventricular dysfunction, provoked by rapid ventricular rate. While the knowledge of mitochondria advanced in most cardiomyopathies, mitochondrial functio...
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Article
Targeted therapies for cardiac diseases
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 predispos...
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Open AccessMitochondria as Therapeutic Targets in Heart Failure
We review therapeutic approaches aimed at restoring function of the failing heart by targeting mitochondrial reactive oxygen species (ROS), ion handling, and substrate utilization for adenosine triphosphate (A...
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Article
A pathophysiological compass to personalize antianginal drug treatment
Myocardial ischaemia results from coronary macrovascular or microvascular dysfunction compromising the supply of oxygen and nutrients to the myocardium. The underlying pathophysiological processes are manifold...
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Open AccessHaematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling
While classical cannabinoid receptors are known to crucially impact on myocardial infarction (MI) repair, a function of the cannabinoid-sensitive receptor GPR55 herein is poorly understood. We investigated the...
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Open AccessCellular and mitochondrial mechanisms of atrial fibrillation
The molecular mechanisms underlying atrial fibrillation (AF), the most common form of arrhythmia, are poorly understood and therefore target-specific treatment options remain an unmet clinical need. Excitation...
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Open AccessTherapeutic approaches in heart failure with preserved ejection fraction: past, present, and future
In contrast to the wealth of proven therapies for heart failure with reduced ejection fraction (HFrEF), therapeutic efforts in the past have failed to improve outcomes in heart failure with preserved ejection ...
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Open AccessSelective NADH communication from α-ketoglutarate dehydrogenase to mitochondrial transhydrogenase prevents reactive oxygen species formation under reducing conditions in the heart
In heart failure, a functional block of complex I of the respiratory chain provokes superoxide generation, which is transformed to H2O2 by dismutation. The Krebs cycle produces NADH, which delivers electrons to c...
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