Publications by authors named "G M Brenner"
Background: Cardiac remodelling, a crucial aspect of heart failure, is commonly investigated in preclinical models by quantifying cardiomyocyte cross-sectional area (CSA) and microvascular density (MVD) via histological methods, such as immunohistochemistry. To achieve this, optimized protocols are needed, and the species specificity is dependent on the antibody used. Lectin histochemistry offers several advantages compared to antibody-based immunohistochemistry, including as cost-effectiveness and cross-species applicability.
View Article and Find Full Text PDFBackground And Purpose: MicroRNA (miRNA) therapy is a promising approach to induce cardioprotection. We have previously identified cardiac microRNA-125b* (microRNA-125b-2-3p; miR-125b*) as a potential cardioprotective miRNA, termed ProtectomiR. We aimed to characterize the pharmacokinetics and pharmacodynamics, and the effect of miR-125b* mimic on infarct size using an in vivo mouse model.
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- - The study aimed to create a simpler mouse model of heart failure with reduced ejection fraction (HFrEF) using angiotensin-II treatment, comparing it to the traditional TAC model, which requires more skilled surgery and longer monitoring time.
- - Analysis included mortality rates, heart function, structural changes, and gene expression, with statistical comparisons made between the two models to understand their similarities and differences.
- - Results showed that while both models exhibited declines in heart function, the Ang-II treatment resulted in less heart dilation and hypertrophy compared to the TAC model, yet their molecular changes were strongly correlated.
Article Synopsis
- * In experiments with mice, SGLT2 knockout mice showed only mild heart dysfunction, while EMPA significantly improved heart function and reduced fibrosis, edema, and oxidative stress in both normal and SGLT2 knockout mice.
- * The study suggests that EMPA's protective effects come from its interaction with the sodium hydrogen exchanger 1 (NHE1) and nitric oxide (NO) pathways rather than through SGLT2 inhibition, highlighting the importance of targeting NHE1 for heart failure treatment. *
Hypercholesterolemia (HC) induces, propagates and exacerbates cardiovascular diseases via various mechanisms that are yet not properly understood. Extracellular vesicles (EVs) are involved in the pathomechanism of these diseases. To understand how circulating or cardiac-derived EVs could affect myocardial functions, we analyzed the metabolomic profile of circulating EVs, and we performed an in-depth analysis of cardiomyocyte (CM)-derived EVs in HC.
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