Special Issue "Advances in the Management of Diabetic Nephropathy"
Deadline for manuscript submissions: 31 December 2021.
Interests: kidney fibrosis; diabetic nephropathy; microRNAs in kidneys; molecular and cellular basis of diabetic kidney disease; glomerular diseases; diabetic endothelium and organelle crosstalk in kidneys
Diabetic nephropathy is a serious kidney-related complication of diabetes mellitus. About 25% of people with diabetes eventually develop kidney disease, and diabetes is also a leading cause of end-stage renal disease. The molecular and cellular basis of this renal disease is poorly understood, and this knowledge gap contributes to the suboptimal treatment options available for these patients. Improved understanding of the pathogenesis of diabetic nephropathy is urgently needed to catalyze the development of novel therapeutics. Current therapeutic regimens for these patients include ACE inhibitors, ARBs, and statins that can minimize the effects of the illness but not prevent it. However, side effects to these agents often exceed their overall efficacy. Thus, there is a clear medical need for new therapeutic strategies to improve kidney function in diabetic patients. In this Special Issue of Pharmaceuticals, we are inviting original as well as review articles to deepen our insight into the new pathophysiologic pathways, mechanisms, and advances in therapeutic approaches in the management of diabetic nephropathy.
Dr. Swayam Prakash Srivastava
Dr. Surya Pandey
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceuticals is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- diabetic nephropathy
- kidney fibrosis
- microRNAs in kidneys
- new therapeutic approaches in the management of diabetic kidney disease
- glomerular diseases
- diabetic endothelium
- organelle crosstalk in kidneys
- mitochondrial-targeted therapy
- molecular and cellular basis of diabetic kidney disease
- chronic kidney disease
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Molecular Mechanisms of Renal Effect of Liraglutide on Cellular Model of Proximal Tubular Cells
Authors: Vjera Nincevic; Tea Omanovic Kolaric; Martina Smolic; Tomislav Kizivat; Milorad Zjalic; Lucija Kuna; Aleksandar Vcev; Ines Bilic Curcic
Affiliation: Faculty of Dental medicine and health Osijek, Faculty of Medicine Osijek
Abstract: Diabetic nephropathy (DN) is a major complication of diabetes mellitus both type I and II, possibly leading to end-stage renal disease. Majority of the DN research is focused on glomeruli, however, most recent studies show important role of tubules in the progression of the disease. Key extracellular conditions that contribute to proximal tubular damage in DN include hyperglycemia, proteinuria, hypoxia, and inflammation acting through hormone-induced release of cytokines (TGF-β), the renin-angiotensin system, and dysregulation of pathways such as polyol pathways. Hyperglycemia promotes cellular hypertrophy and collagen gene transcription and can stimulate the interstitial fibroblasts to increase their synthesis of fibrillar collagens and extracellular matrix (ECM) via an autocrine TGF-β1 system. In addition, mechanisms through which hypoxia causes tubular damage includes oxidative stress, inflammation, and matrix production. Long acting glucagone like protein receptor agonists (GLP-1 RA) have demostrated significant renoprotective effects in clinical studies but the mechanisms involved remain elusive. The aim of this research was to determine the viability of cells in tubular damage, to measure the effects of TGF- β and the expression of major genes involved in signal transduction pathways of tubular damage in in vitro model of DN and to assess the effect of liraglutide on gene expression involved in signaling pathways of tubular damage. Identifying new potential target molecules and molecular pathways could lead to development of new specific therapeutic options for DN prevention and treatment.