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      RELEVANCE OF TNF-α IN THE CONTEXT OF OTHER INFLAMMATORY CYTOKINES IN THE PROGRESSION OF DIABETIC NEPHROPATHY

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      Author(s): 1 , 2
      Publication date PMC-release:
      Journal: Kidney international
      Keywords: Diabetic Nephropathy, Inflammatory Cytokines

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          Abstract

          An ancillary paradigm that has evolved recently in the pathogenesis of diabetic nephropathy includes subclinical “micro-inflammation” with influx of macrophages and consequential generation of myriad pro-inflammatory cytokines and ensuing kidney damage. Among various pro-inflammatory cytokines TNF-α has attracted the most attention since it amplifies the inflammatory network of cytokines leading to worsening of the progression of diabetic nephropathy. The accompanying article by Awad et al. examines the role of TNF-α in the pathogenesis of experimental diabetic nephropathy.

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          A glimpse of various pathogenetic mechanisms of diabetic nephropathy.

          Yashpal S Kanwar, Lin Sun, Ping Xie … (2011)
          Diabetic nephropathy is a well-known complication of diabetes and is a leading cause of chronic renal failure in the Western world. It is characterized by the accumulation of extracellular matrix in the glomerular and tubulointerstitial compartments and by the thickening and hyalinization of intrarenal vasculature. The various cellular events and signaling pathways activated during diabetic nephropathy may be similar in different cell types. Such cellular events include excessive channeling of glucose intermediaries into various metabolic pathways with generation of advanced glycation products, activation of protein kinase C, increased expression of transforming growth factor β and GTP-binding proteins, and generation of reactive oxygen species. In addition to these metabolic and biochemical derangements, changes in the intraglomerular hemodynamics, modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-induced injury. Events involving various intersecting pathways occur in most cell types of the kidney.
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            Inflammation in Diabetic Nephropathy

            Andy K. H. Lim, Gregory Tesch (2012)
            Diabetic nephropathy is the leading cause of end-stage kidney disease worldwide but current treatments remain suboptimal. This review examines the evidence for inflammation in the development and progression of diabetic nephropathy in both experimental and human diabetes, and provides an update on recent novel experimental approaches targeting inflammation and the lessons we have learned from these approaches. We highlight the important role of inflammatory cells in the kidney, particularly infiltrating macrophages, T-lymphocytes and the subpopulation of regulatory T cells. The possible link between immune deposition and diabetic nephropathy is explored, along with the recently described immune complexes of anti-oxidized low-density lipoproteins. We also briefly discuss some of the major inflammatory cytokines involved in the pathogenesis of diabetic nephropathy, including the role of adipokines. Lastly, we present the latest data on the pathogenic role of the stress-activated protein kinases in diabetic nephropathy, from studies on the p38 mitogen activated protein kinase and the c-Jun amino terminal kinase cell signalling pathways. The genetic and pharmacological approaches which reduce inflammation in diabetic nephropathy have not only enhanced our understanding of the pathophysiology of the disease but shown promise as potential therapeutic strategies.
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              Inflammatory Cytokines in Diabetic Nephropathy

              Javier Donate-Correa, Ernesto Martín-Núñez, Mercedes Muros de Fuentes … (2015)
              Probably, the most paradigmatic example of diabetic complication is diabetic nephropathy, which is the largest single cause of end-stage renal disease and a medical catastrophe of worldwide dimensions. Metabolic and hemodynamic alterations have been considered as the classical factors involved in the development of renal injury in patients with diabetes mellitus. However, the exact pathogenic mechanisms and the molecular events of diabetic nephropathy remain incompletely understood. Nowadays, there are convincing data that relate the diabetes inflammatory component with the development of renal disease. This review is focused on the inflammatory processes that develop diabetic nephropathy and on the new therapeutic approaches with anti-inflammatory effects for the treatment of chronic kidney disease in the setting of diabetic nephropathy.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 0323470
                Journal ID (pubmed-jr-id): 5428
                Journal ID (nlm-ta): Kidney Int
                Journal ID (iso-abbrev): Kidney Int.
                Title: Kidney international
                ISSN (Print): 0085-2538
                ISSN (Electronic): 1523-1755
                Publication date Nihms-submitted: 6 August 2015
                Publication date (Print): October 2015
                Publication date PMC-release: 01 April 2016
                Volume: 88
                Issue: 4
                Pages: 662-665
                Affiliations
                [1 ]Department of Nephrology & Renal Institute, 2nd Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China
                [2 ]Departments of Pathology & Medicine, Northwestern University, Chicago, IL, USA
                Author notes
                Correspondence address: Yashpal S. Kanwar, M.D., PhD, Department of Pathology, Northwestern University Medical School, 303 E. Chicago Ave, Chicago, Illinois 60611, (312) 503-0004, (312) 503-0627, y-kanwar@ 123456northwestern.edu , Lin SUN, M.D., Ph.D, Department of Nephrology, The Second Xiangya Hospital, Kidney Institute of Nephrology, Central South University, Changsha, Hunan Province 410011, China, (731) 8529-2064, sunlinnwu11@ 123456163.com
                Article
                Manuscript ID: NIHMS710449
                DOI: 10.1038/ki.2015.250
                PMC ID: 4589869
                PubMed ID: 26422621
                SO-VID: 503604d5-2ba7-4374-81c1-bf9227c8a501
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                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

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                Subject: Article

                ScienceOpen disciplines: Nephrology
                Keywords: diabetic nephropathy,inflammatory cytokines
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: diabetic nephropathy, inflammatory cytokines

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