Abstract
Abstract The over-produced reactive oxygen species (ROS) and reactive nitrogen species (RNS) in inflammatory diseases, such as neurodegenerative diseases, Type 2 diabetes (T2D), cardiovascular injury and autoimmune disease, would accompany a significant increase in protein tyrosine nitration that attributes to initiation and progression of these diseases. Understanding the most biologically relevant nitration pathways in vivo, identifying nitration sites of the specific nitrated proteins, and unveiling the nitration-induced biological consequences would provide invaluable information for the clinical understandingly of onset and progression of the associated diseases and also for the design of clinical interventions by catalytically decomposing and scavenging RNS/ROS for prevention of protein nitration in vivo.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
