Skip to main content Skip to main navigation menu Skip to site footer

The involvement of proinflammatory cytokines in diabetic nephropathy: Focus on interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α) signaling mechanism

Abstract

About 20-40% of type 2 diabetic patients may develop diabetic nephropathy (DN) as its complication. The pathogenesis of DN is a complex one. Classically, metabolic and hemodynamic impairment are considered as its pathogenesis. This view has evolved tremendously in recent years. Large number of evidences points that inflammation is a key event in the development and progression of DN. Among several inflammatory molecules, proinflammatory cytokines such as interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α) are known to be involved. Chronic condition of hyperglycemia responsible for the formation of proinflammatory cytokines via advanced glycation end products (AGE) pathway and protein kinase C (PKC) pathway. These proinflammatory cytokines exert signaling pathway that lead to extracellular matrix (ECM) accumulation, glomerular basement membrant (GBM) thickening, and glomerulosclerosis, ultimately lead to development and progression of diabetic nephropathy. Knowing this mechanism in detail beneficial for future treatment. Intervention in these signaling pathway may benefit to development of novel therapeutic approach.

How to Cite

Sindhughosa, D. A., & Pranamartha, A. G. M. K. (2017). The involvement of proinflammatory cytokines in diabetic nephropathy: Focus on interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α) signaling mechanism. Bali Medical Journal, 6(1), 44–51. https://doi.org/10.15562/bmj.v6i1.299

HTML
0

Total
1

Share

Search Panel

Dwijo Anargha Sindhughosa
Google Scholar
Pubmed
BMJ Journal


AA Gde Marvy Khrisna Pranamartha
Google Scholar
Pubmed
BMJ Journal