In vıtro fare ve ın vıvo zebrafısh modelleri ile farklı diyetlerin anjiyogeneze etkisi

Cardiovascular disorders rank as the primary cause of global mortality. Being overweight or obese impacts the pathogenesis of cardiovascular disease, resulting in an imbalance in endothelial function, cell growth, and inflammatory activation (Shrestha et al. 2020). Disruption of these factors resulting from endothelial cell dysfunction serves as both an outcome and a catalyst for vascular disease processes. Endothelial cells (ECs) are a natural barrier between circulating blood and vessel components. They also play critical roles in multiple physiological and pathophysiological processes, such as angiogenesis, vascular permeability, and inflammation. Amelioration of endothelial dysfunction may be attained by weight loss; however, complementary in vitro and in vivo studies are needed to establish the effects of weight loss on endothelial function and angiogenesis. This study developed an in vitro model to understand better the diet-induced changes in angiogenesis for mouse endothelial cells. In addition, a novel in vivo model of diet-induced vascular dysfunction and its reversal with a regular diet in a zebrafish model was also studied. In this study, in vitro studies show that a high-fat diet (HFD) has a proliferative effect on endothelial cells and weight loss does not compensate for prior stress induced by HFD. In vivo studies showed that an egg yolk-based high-fat diet might affect hepatic and angiogenesis parameters, on which weight loss partially affects both larvae and adult zebrafish. These preclinical models can be helpful experimental models to study diet-induced changes in angiogenesis and regeneration under different dietary regimes.