Angiologia: Acesso Aberto
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Linking Cancer to Metabolic Syndrome through it’s Individual Contributory Components: Oxidative Stress and Renin-Angiotensin-Aldosterone Axis Dysregulation

Chirag H Mandavia

Impaired signaling pathways as a result of the increased oxidative stress and general metabolic dysregulation seen in metabolic syndrome may contribute to the increased cancer risk seen in otherwise healthy patients; and subsequent development of progressive cancer characterized by metastatic process. Oxidative stress leading to insulin resistance is a major component of the metabolic syndrome. Dysregulation of the Renin-Angiotensin-Aldosterone (RAAS) axis is known to be one of the major risk factors for metabolic syndrome; and recently has been shown to play a significant contributory role in the development of oxidative stress; leading up to insulin resistance; in the metabolic syndrome by several different groups. In recent years; angiotensin and aldosterone have emerged as important contributory pathogenic factors for the development of metabolic syndrome; primarily through their ability to cause cellular oxidative stress. Angiotensin (Ang II) can also induce oxidative stress through activation of NADPH oxidase. Recently; metabolic syndrome has been associated with increased risk for a variety of cancers. Since oxidative stress is a critical component of the metabolic syndrome; it stands to reason that Ang II excess would increase oxidative stress and contribute further to increased cancer risk in terms of epigenetic dysregulation in stressed cells. Thus the purpose of this study is to check the effect of the RAAS axis on cancer development and characterize the intracellular signaling pathways involved. Specifically; the correlation of cancer incidence and spread to Ang II treatment and levels of oxidative stress will allow us to analyze the role of the vital contributory components of the metabolic syndrome in cancer.