作者: Monisha Dhiman , Shweta Thakur , Shishir Upadhyay , Amandeep Kaur , Anil K. Mantha
DOI: 10.1007/978-81-322-2035-0_17
关键词: Bioinformatics 、 Endothelial dysfunction 、 Disease 、 Diabetes mellitus 、 Oxidative stress 、 Oxidative phosphorylation 、 Nitric oxide 、 Inflammation 、 Reactive oxygen species 、 Medicine
摘要: Globally, the major cause of long-term disability and death is an “epidemiologic transition” from infectious diseases malnutrition complications to non-communicable chronic like cardiovascular disease (CVD), cancer diabetes. CVD accounts for global mortality. Imbalance due generation reactive oxygen species (ROS) levels above normal baseline decreased antioxidant defence reserve makes system (cardiac vascular cells) susceptible oxidative stress damage. Growing evidences support notion that plays a crucial role in development progression by altering functions such as inactivation nitric oxide (NO) leading endothelial dysfunction, intracellular Ca2+ overload others. Oxidative also mediates inflammation through various signalling cascades activation inflammatory transcription factors (TFs) namely NF-κB, AP-1 Nrf-1. A vicious cycle stress-mediated inflammation-induced CVD-related worse. Therefore, it very important clearly understand enzymatic sources ROS, mechanisms underlying pathological conditions link between during each stage CVD. The present chapter will elucidate progression. It find remedial measures, develop efficient biomarkers design therapeutic strategies near future.