+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      NF-κβ: A Potential Target in the Management of Vascular Complications of Diabetes


      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          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.

          Related collections

          Most cited references112

          • Record: found
          • Abstract: not found
          • Article: not found

          Diabetic Neuropathies: A statement by the American Diabetes Association

            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            TGF-β/Smad signaling in renal fibrosis

            TGF-β (transforming growth factor-β) is well identified as a central mediator in renal fibrosis. TGF-β initiates canonical and non-canonical pathways to exert multiple biological effects. Among them, Smad signaling is recognized as a major pathway of TGF-β signaling in progressive renal fibrosis. During fibrogenesis, Smad3 is highly activated, which is associated with the down-regulation of an inhibitory Smad7 via an ubiquitin E3-ligases-dependent degradation mechanism. The equilibrium shift between Smad3 and Smad7 leads to accumulation and activation of myofibroblasts, overproduction of ECM (extracellular matrix), and reduction in ECM degradation in the diseased kidney. Therefore, overexpression of Smad7 has been shown to be a therapeutic agent for renal fibrosis in various models of kidney diseases. In contrast, another downstream effecter of TGF-β/Smad signaling pathway, Smad2, exerts its renal protective role by counter-regulating the Smad3. Furthermore, recent studies demonstrated that Smad3 mediates renal fibrosis by down-regulating miR-29 and miR-200 but up-regulating miR-21 and miR-192. Thus, overexpression of miR-29 and miR-200 or down-regulation of miR-21 and miR-192 is capable of attenuating Smad3-mediated renal fibrosis in various mouse models of chronic kidney diseases (CKD). Taken together, TGF-β/Smad signaling plays an important role in renal fibrosis. Targeting TGF-β/Smad3 signaling may represent a specific and effective therapy for CKD associated with renal fibrosis.
              • Record: found
              • Abstract: found
              • Article: not found

              Diabetic retinopathy: seeing beyond glucose-induced microvascular disease.

              Diabetic retinopathy remains a frightening prospect to patients and frustrates physicians. Destruction of damaged retina by photocoagulation remains the primary treatment nearly 50 years after its introduction. The diabetes pandemic requires new approaches to understand the pathophysiology and improve the detection, prevention, and treatment of retinopathy. This perspective considers how the unique anatomy and physiology of the retina may predispose it to the metabolic stresses of diabetes. The roles of neural retinal alterations and impaired retinal insulin action in the pathogenesis of early retinopathy and the mechanisms of vision loss are emphasized. Potential means to overcome limitations of current animal models and diagnostic testing are also presented with the goal of accelerating therapies to manage retinopathy in the face of ongoing diabetes.

                Author and article information

                Front Pharmacol
                Front Pharmacol
                Front. Pharmacol.
                Frontiers in Pharmacology
                Frontiers Media S.A.
                07 November 2017
                : 8
                : 798
                [1]Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM’s Narsee Monjee Institute of Management Studies , Mumbai, India
                Author notes

                Edited by: Cristiano Fava, University of Verona, Italy

                Reviewed by: Elisa Danese, University of Verona, Italy; Angela Tagetti, University of Verona, Italy; Melania Dovizio, Università degli Studi “G. d’Annunzio” Chieti - Pescara, Italy

                *Correspondence: Yogesh A. Kulkarni, yogeshkulkarni101@ 123456yahoo.com

                This article was submitted to Inflammation Pharmacology, a section of the journal Frontiers in Pharmacology

                Copyright © 2017 Suryavanshi and Kulkarni.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                : 11 June 2017
                : 23 October 2017
                Page count
                Figures: 4, Tables: 0, Equations: 0, References: 153, Pages: 12, Words: 0

                Pharmacology & Pharmaceutical medicine
                nf-κβ,diabetic complications,inflammation,nephropathy,neuropathy,retinopathy,cardiomyopathy,nf-κβ inhibitors


                Comment on this article