Abstract
Cardiovascular disease (CVD) encompasses a range of conditions affecting the cardiovascular system, including complications such as heart attacks and hypertension. As a leading global health concern and the primary contributor to mortality worldwide, understanding the mechanisms underlying CVD is critical due to its profound impact on individuals and society. This study explores the intricate landscape of CVD, focusing on key signaling proteins associated with heart attacks and hypertension. The findings highlight nine proteins (transforming growth factor beta 1, apolipoprotein E, nitric oxide synthase 3, plasminogen activator-tissue, interleukin 6, tumor necrosis factor, glycogen synthase kinase 3 beta, matrix metalloproteinase 9, and angiotensinogen) that are commonly implicated in pathways linked to these conditions, playing essential roles in physiological processes and contributing to the pathogenesis of CVD. In addition, the study emphasizes the significance of oncogenes and tumor suppressor genes in cardiovascular signaling pathways, identifying androgen receptor (AR), guanine nucleotide-binding protein, alpha stimulating (GNAS), and tumor protein p53 as critical contributors. Dysregulation of AR is linked to hypertension, atherosclerosis, and heart failure, underscoring its potential as a therapeutic target. Similarly, GNAS mutations disrupt signal transduction, impair heart function, and contribute to arteriosclerosis and hypertension. By examining the interplay between signaling proteins, oncogenes, and suppressor genes, this study offers valuable insights into the molecular mechanisms driving CVD. The identified targets provide promising opportunities for future studies aimed at developing targeted therapies for CVD.
Published Version
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