inflammation in the pathogenesis of microvascular complications in diabetes

Clicks: 165
ID: 199521
2012
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Abstract
Diabetes and hyperglycemia create a proinflammatory microenvironment that progresses to microvascular complications such as nephropathy, retinopathy, and neuropathy. Diet-induced insulin resistance is a potential initiator of this change in Type 2 diabetes (T2D) which can increase adipokines and generate a chronic low-grade inflammatory state. The advanced glycation end-products (AGEs) AGE receptor (RAGE) axis, reactive oxygen species, and hypoxia can also interact to worsen complications. Numerous efforts have gained way to understanding the mechanisms of these modulators and attenuation of the inflammatory response, however effective treatments have still not emerged. The complexity of inflammatory signaling may suggest a need for multi-targeted therapy. This review presents recent findings aimed at new treatment strategies.
Reference Key
nguyen2012frontiersinflammation Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Dung Van Nguyen;Lynn eShaw;Maria eGrant
Journal aip advances
Year 2012
DOI
10.3389/fendo.2012.00170
URL
http://journal.frontiersin.org/Journal/10.3389/fendo.2012.00170/full
Keywords
inflammation diabetes mellitus oxidative stress inflammatory cytokines advanced glycation end-products clinical endocrinology

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