Publications by authors named "D Belke"
Article Synopsis
- * Researchers identified 21 human ITPR1 GOF variants and created a mouse model with one of these variants (ITPR1-W1457G), which was found to be prone to stress-induced ventricular arrhythmias.
- * Both mouse models and human data suggest that ITPR1 GOF variants increase Ca handling abnormalities and arrhythmia risk, with 7 rare ITPR1 variants in a human database showing similar GOF behavior linked to cardiac
Article Synopsis
- Human pericardial fluid (PF) contains biologically active markers that have significant effects on heart-related cellular activities.
- PF can enhance the activity of cardiac fibroblasts, which are important for heart tissue repair, through a specific biological pathway known as the transforming growth factor-β pathway.
- In patients with coronary artery disease, the PF possesses a higher capacity to promote fibrosis compared to those without the disease, indicating a potential area for clinical attention.
Background: Pericardial fluid (PF) contains cells, proteins, and inflammatory mediators, such as cytokines, chemokines, growth factors, and matrix metalloproteinases. To date, we lack an adequate understanding of the inflammatory response that acute injury elicits in the pericardial space.
Objective: To characterize the inflammatory profile in the pericardial space acutely after ischemia/reperfusion.
Objective: This study tested the hypothesis that administration of the KCa channel activator SKA-31 restores endothelium-dependent vasodilation in vivo in Type 2 Diabetic (T2D) rats.
Background: Acute treatment of isolated resistance arteries from T2D rats and humans with SKA-31 significantly improved endothelium-dependent vasodilation. However, it is unknown whether these in situ actions translate to intact vascular beds in vivo.
Background: Aging is a major risk factor for atrial fibrillation (AF); however, not all individuals age at the same rate. Frailty, which is a measure of susceptibility to adverse health outcomes, can be quantified with a frailty index (FI).
Objective: This study aimed to determine the effects of angiotensin-converting enzyme (ACE) inhibition on AF and atrial remodeling in aging and frail mice.