Engaging novel cell types, protein targets and efficacy biomarkers in the treatment of diabetic nephropathy.

Ryan M Fryer,Carine M Boustany-Kari,Scott M Macdonnell

doi:10.3389/fphar.2014.00185

Ryan M Fryer, Carine M Boustany-Kari + Show 1 more

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https://doi.org/10.3389/fphar.2014.00185

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Abstract

EDITORIAL article Front. Pharmacol., 07 August 2014Sec. Experimental Pharmacology and Drug Discovery https://doi.org/10.3389/fphar.2014.00185

Highlights

Diabetic nephropathy (DN) is a well-known complication of diabetes and leading cause of chronic renal failure and end-stage renal disease (ESRD)
Can a population of inflammatory cells be targeted to slow disease progression? Or, should we look more closely to podocyte-selective targets central to the regulation of glomerular filtration? Alternatively, do we set our sights within the complicated environment of the renal microvasculature? While early DN may represent an overtly angiogenic environment, advanced disease likely represents a condition of capillary loss and excess anti-angiogenic activity (Advani and Gilbert, 2012)
In this Research Topic, contributing authors explored four sub-areas within the realm of chronic kidney disease and DN including capitalizing on the discovery of novel mineralocorticoid receptors with potentially lesser risk for hyperkalemia (Orena et al, 2013), the potential for modulation of a secreted glycoprotein already recognized as a contributor to minimal change disease and as a target in DN (Chugh et al, 2014), use of an endogenous anti-fibrotic peptide in renal disease (Kanasaki et al, 2014), and basic science that investigated the expression of mitogen-activated protein kinases (MAPKs) in podocytes as potential new targets in DN (Badshah et al, 2014), an interesting area that may offer another pathway and novel players for targeted therapies in this disease

Summary

Introduction

Diabetic nephropathy (DN) is a well-known complication of diabetes and leading cause of chronic renal failure and end-stage renal disease (ESRD). Various signaling pathways encompassing inflammation, fibrosis, and oxidative stress are implicated in the pathogenesis of DN (Reidy et al, 2014) and perhaps the key to novel and efficacious therapies lays within the identification of druggable targets that encompass these diverse processes.

Results

Conclusion