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Heart-type fatty acid binding protein (FABP3) is an effective biomarker for cardiac injuries. However, it has also been tested as a biomarker in patients with peripheral artery diseases; these conditions are complications of atherosclerosis, which is driven by endothelial dysfunction. As FABP3 release is not exclusive to the heart but appears to characterize cardiovascular events, whether FABP3 influences endothelial function is not known. Additionally, the transcriptomic profiles of endothelial cells during cardiovascular stresses remain under-investigated. This thesis investigates the multifaceted role of FABP3 and the transcriptomic alterations in endothelial cells under different cardiovascular stressors, offering novel insights into endothelial dysfunction and atherosclerosis. Through a series of in vitro studies, the regulatory dynamics of FABP3 under atherosclerotic stressors, its impact on endothelial cell gene expression, and the effects of Angiotensin II (Ang II) exposure on coding and long noncoding RNAs were demonstrated. The findings of this thesis reveal that FABP3 expression is differentially modulated by oxidative stress, inflammation, and hypertension and highlight its therapeutic potential in cardiovascular diseases through loss of function studies. Additionally, transcriptomic profiling uncovers significant changes in messenger RNAs and long non-coding RNAs, identifying novel pathways involved in endothelial response to Ang II-induced stress. This comprehensive analysis advances the understanding of the molecular mechanisms underlying endothelial dysfunction and opens new avenues for research on intervention in endothelial …