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. 2012 Dec 21:3:170.
doi: 10.3389/fendo.2012.00170. eCollection 2012.

Inflammation in the pathogenesis of microvascular complications in diabetes

Dung V Nguyen  1 , Lynn C Shaw, Maria B Grant
Affiliations

Inflammation in the pathogenesis of microvascular complications in diabetes

Dung V Nguyen et al. Front Endocrinol (Lausanne). .

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 which can increase adipokines and generate a chronic low-grade inflammatory state. Advanced glycation end-products and its receptor, glycation end-products AGE receptor 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.

Keywords: advanced glycation end-products; diabetes mellitus; inflammation; inflammatory cytokines; microvascular complications; oxidative stress.

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Figures

FIGURE 1
FIGURE 1
General pathway in the progression of diabetic microvascular complications.
FIGURE 2
FIGURE 2
Activation of RAS can lead to progressive or protective effects depending on the signaling mechanisms.
See this image and copyright information in PMC

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