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  3. Activation of common signaling pathways during remodeling of the heart and the bladder

Activation of common signaling pathways during remodeling of the heart and the bladder

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DOI
10.7892/boris.75187
Publisher DOI
10.1016/j.bcp.2015.09.012
PubMed ID
26390804
Abstract
The heart and the urinary bladder are hollow muscular organs, which can be afflicted by pressure overload injury due to pathological conditions such as hypertension and bladder outlet obstruction. This increased outflow resistance induces hypertrophy, marked by dramatic changes in the organs' phenotype and function. The end result in both the heart and the bladder can be acute organ failure due to advanced fibrosis and the subsequent loss of contractility. There is emerging evidence that microRNAs (miRNAs) play an important role in the pathogenesis of heart failure and bladder dysfunction. MiRNAs are endogenous non-coding single-stranded RNAs, which regulate gene expression and control adaptive and maladaptive organ remodeling processes. This Review summarizes the current knowledge of molecular alterations in the heart and the bladder and highlights common signaling pathways and regulatory events. The miRNA expression analysis and experimental target validation done in the heart provide a valuable source of information for investigators working on the bladder and other organs undergoing the process of fibrotic remodeling. Aberrantly expressed miRNA are amendable to pharmacological manipulation, offering an opportunity for development of new therapies for cardiac and bladder hypertrophy and failure.
Date Issued
2016
Publication Type
Article
Subject(s)
600 Technology > 610 Medicine & health
Subjects
Bladder
•
Fibrosis
•
Gene expression
•
Heart
•
Obstruction
•
Pressure overload
•
Signaling
•
miRNA
Language(s)
en
Author(s)
Köck, Ivonne  
Departement Klinische Forschung, Forschungsgruppe Urologie  
Burkhard, Fiona Christine  
Universitätsklinik für Urologie  
Monastyrskaya-Stäuber, Katia  
Departement Klinische Forschung, Forschungsgruppe Urologie  
Additional Credits
Departement Klinische Forschung, Forschungsgruppe Urologie  
Universitätsklinik für Urologie  
Journal
Biochemical pharmacology
Publisher
Elsevier
ISSN
0006-2952
Access(Rights)
restricted
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