Abstract
Diabetes is a metabolic disorder affecting large percentage of population worldwide. NF-κβ plays key role in pathogenesis of vascular complications of diabetes. Persistent hyperglycemia activates NF-κβ that triggers expression of various cytokines, chemokines and cell adhesion molecules. Over-expression of TNF-α, interleukins, TGF-β, Bcl2 and other pro-inflammatory proteins and pro-apoptotic genes by NF-κβ is key risk factor in vascular dysfunction. NF-κβ over-expression also triggers calcification of endothelial cells leading to endothelial dysfunction and further vascular complications. Inhibition of NF-κβ pro-inflammatory pathway is upcoming novel target for management of vascular complications of diabetes. Various natural and synthetic inhibitors of NF-κβ have been studied in management of diabetic complications. Recent preclinical and clinical studies validate NF-κβ as promising target in the management of vascular complications of diabetes.
Highlights
Diabetes mellitus (DM) and its associated complications are one of the major leading causes of mortality in public worldwide (IDF, 2015; WHO, 2016)
The current review focuses on role of nuclear factor-κβ (NF-κβ) in pathophysiology of various vascular complications of diabetes and effect of NF-κβ inhibitors in the management of same
Various preclinical studies have been carried out to study the effect of natural NF-κβ inhibitors in the management of diabetic complications; but its implication in clinical setting is limited
Summary
Diabetes mellitus (DM) and its associated complications are one of the major leading causes of mortality in public worldwide (IDF, 2015; WHO, 2016). It inhibited degradation of NF-κβ regulatory protein IκBα leading to decreased expression of pro-inflammatory (TNF-α, IL1β) and profibrotic cytokines (ICAM-1, MCP-1, and TGF-β1) (Soetikno et al, 2011). Treatment with piceatannol inhibited NF-kB p65/p50 binding to DNA and reduced renal pro-inflammatory cytokines like TNF-α, IL-1β and IL-6 (Borgohain et al, 2017).
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
