Chang, M.-Y. and C.M. Ong, A. (2018) Targeting new cellular disease pathways in autosomal dominant polycystic kidney disease. Nephrology Dialysis Transplantation, 33 (8). pp. 1310-1316. ISSN 0931-0509
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of end-stage renal failure. Understanding the molecular and cellular pathogenesis of ADPKD could help to identify new targets for treatment. The classic cellular cystic phenotype includes changes in proliferation, apoptosis, fluid secretion, extracellular matrix and cilia function. However, recent research, suggests that the cellular cystic phenotype could be broader and that changes, such as altered metabolism, autophagy, inflammation, oxidative stress and epigenetic modification, could play important roles in the processes of cyst initiation, cyst growth or disease progression. Here we review these newer cellular pathways, describe evidence for their possible links to cystic pathogenesis or different stages of disease and discuss the options for developing novel treatments.
Metadata
Item Type: | Article |
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Authors/Creators: |
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Copyright, Publisher and Additional Information: | © 2017 The Author. This is an author-produced version of a paper subsequently published in Nephrology Dialysis Transplantation. Uploaded in accordance with the publisher's self-archiving policy. |
Keywords: | Animals; Epigenesis, Genetic; Extracellular Matrix; Humans; Inflammation; Metabolic Networks and Pathways; Polycystic Kidney, Autosomal Dominant |
Dates: |
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Institution: | The University of Sheffield |
Academic Units: | The University of Sheffield > Faculty of Medicine, Dentistry and Health (Sheffield) > School of Medicine and Population Health |
Funding Information: | Funder Grant number EUROPEAN COMMISSION - FP6/FP7 TRANCYST - 317246 |
Depositing User: | Symplectic Sheffield |
Date Deposited: | 24 Nov 2023 12:41 |
Last Modified: | 24 Nov 2023 20:00 |
Status: | Published |
Publisher: | Oxford University Press (OUP) |
Refereed: | Yes |
Identification Number: | 10.1093/ndt/gfx262 |
Related URLs: | |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:205751 |