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Review
. 2014:2014:968681.
doi: 10.1155/2014/968681. Epub 2014 Feb 4.

New insight into the molecular drug target of diabetic nephropathy

Affiliations
Review

New insight into the molecular drug target of diabetic nephropathy

Vivian Soetikno et al. Int J Endocrinol. 2014.

Abstract

Diabetic nephropathy (DN) lowered quality of life and shortened life expectancy amongst those affected. Evidence indicates interaction between advanced glycation end products (AGEs), activated protein kinase C (PKC) and angiotensin II exacerbate the progression of DN. Inhibitors of angiotensin-converting enzyme (ACEIs), renin angiotensin aldosterone system (RAAS), AGEs, and PKC have been tested for slowing down the progression of DN. The exact molecular drug targets that lead to the amelioration of renal injury in DN are not well understood. This review summarizes the potential therapeutic targets, based on putative mechanism in the progression of the disease.

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Figures

Figure 1
Figure 1
Schematic illustration of the interaction between hemodynamic and metabolic factors in the pathophysiology of diabetic nephropathy.
Figure 2
Figure 2
Current drug targets in diabetic nephropathy. Interrelated derangements in cellular hemodynamic, metabolic, oxidative stress, inflammation; lipid dysfunction, and extracellular matrix accumulation occur in diabetes and lead to diabetic nephropathy. These derangements provide the targets for the development of mechanism based drugs.

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