Publications by authors named "Walaa Fakih"
Aims: Sodium-glucose co-transporter 2 inhibitors (SGLT2i) show a cardioprotective effect in heart failure and myocardial infarction, pathologies often associated with low-grade inflammation. This cross-sectional study aims to investigate whether low-grade inflammation regulates SGLT2 expression and function in human vasculature, heart, and endothelial cells (ECs).
Methods And Results: Human internal thoracic artery (ITA), left ventricle (LV) specimens, and cultured porcine coronary artery ECs were used.
Article Synopsis
- Sodium-glucose co-transporter 2 (SGLT2) inhibitors, like dapagliflozin, may reduce the risk of cardiovascular issues and possibly prevent blood vessel thickening after injury, which is not well understood.
- In a study with male rats, dapagliflozin reduced neointima thickening by 32% compared to control and also impacted vascular responses without altering certain inflammatory and oxidative gene expressions.
- The findings suggest that dapagliflozin works by affecting angiotensin and extracellular nucleotide signaling, indicating SGLT2 inhibitors could be a new approach for addressing vascular restenosis.
Article Synopsis
- Atrial fibrillation (AF) is linked to heart issues and involves changes in heart tissue; this study explores how activated factor X (FXa) impacts this process in atrial endothelial cells and human heart tissues.
- The researchers used cells from pig hearts and human surgical samples, testing for various proteins, gene expressions, and signs of stress and fibrosis in response to FXa.
- Findings showed that FXa boosts harmful responses like oxidative stress and inflammation in atrial cells while reducing protective factors, and these effects can be blocked by specific inhibitors targeting FXa.
Background: COVID-19 is associated with an increased risk of cardiovascular complications. Although cytokines have a predominant role in endothelium damage, the precise molecular mechanisms are far from being elucidated.
Objectives: The present study hypothesized that inflammation in patients with COVID-19 contributes to endothelial dysfunction through redox-sensitive SGLT2 overexpression and investigated the protective effect of SGLT2 inhibition by empagliflozin.
The metabolic syndrome comprises a family of clinical and laboratory findings, including insulin resistance, hyperglycemia, hypertriglyceridemia, low high-density lipoprotein cholesterol levels, and hypertension, in addition to central obesity. The syndrome confers a high risk of cardiovascular mortality. Indeed, metabolic dysfunction has been shown to cause a direct insult to smooth muscle and endothelial components of the vasculature, which leads to vascular dysfunction and hyperreactivity.
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- Traumatic brain injury (TBI) is a significant global health issue, leading to long-term disability and high mortality rates, with immediate physical and structural damage occurring after the injury.
- The secondary injury processes that follow involve complex molecular and biochemical changes, including mitochondrial dysfunction and neuroinflammation, which can result in further neuronal injury.
- Recent research indicates that dietary factors, particularly a western diet high in fats, may worsen TBI outcomes by intensifying these damaging processes and hindering recovery efforts.
Prediabetes is a highly prevalent stage of early metabolic dysfunction that poses a high risk for cardiovascular and cognitive impairment without a clear pathological mechanism. Here, we used a non-obese prediabetic rat model previously developed in our laboratory to examine this mechanism. These rats were subjected to a mild metabolic challenge leading to hyperinsulinemia without hyperglycemia or obesity.
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