Universität zu Köln

Haumann, Sophie, Mueller, Roman-Ulrich ORCID: 0000-0001-6910-0745 and Liebau, Max C. (2020). Metabolic Changes in Polycystic Kidney Disease as a Potential Target for Systemic Treatment. Int. J. Mol. Sci., 21 (17). BASEL: MDPI. ISSN 1422-0067

Full text not available from this repository.

Abstract

Autosomal recessive and autosomal dominant polycystic kidney disease (ARPKD, ADPKD) are systemic disorders with pronounced hepatorenal phenotypes. While the main underlying genetic causes of both ARPKD and ADPKD have been well-known for years, the exact molecular mechanisms resulting in the observed clinical phenotypes in the different organs, remain incompletely understood. Recent research has identified cellular metabolic changes in PKD. These findings are of major relevance as there may be an immediate translation into clinical trials and potentially clinical practice. Here, we review important results in the field regarding metabolic changes in PKD and their modulation as a potential target of systemic treatment.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Haumann, Sophie UNSPECIFIED UNSPECIFIED UNSPECIFIED Mueller, Roman-Ulrich UNSPECIFIED orcid.org/0000-0001-6910-0745 UNSPECIFIED Liebau, Max C. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-321400
DOI:	10.3390/ijms21176093
Journal or Publication Title:	Int. J. Mol. Sci.
Volume:	21
Number:	17
Date:	2020
Publisher:	MDPI
Place of Publication:	BASEL
ISSN:	1422-0067
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language ORTHOLOGOUS MOUSE MODEL; ACID BETA-OXIDATION; AUTOSOMAL-DOMINANT; CYST FORMATION; GLUCOSE-METABOLISM; MTOR INHIBITION; ANIMAL-MODELS; 2-HIT MODEL; CELL-SIZE; PROGRESSION Multiple languages Biochemistry & Molecular Biology; Chemistry, Multidisciplinary Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/32140