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Updated: Apr 3, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Activation of common signaling pathways during remodeling of the heart and the bladder
Ivonne Koeck1, Fiona C Burkhard2, Katia Monastyrskaya3
1Urology Research Laboratory, Department Clinical Research, University of Bern, Switzerland; Graduate School for Cellular and Biomedical Sciences, University of Bern, Switzerland.
Insights
MicroRNAs (miRNAs) are key regulators in pressure overload injury affecting the heart and bladder. Understanding their role in organ remodeling offers new therapeutic targets for cardiac and bladder failure.
Area of Science:
- Cardiovascular Biology
- Urology
- Molecular Biology
Background:
- The heart and urinary bladder are susceptible to pressure overload injury from conditions like hypertension and bladder outlet obstruction.
- This injury leads to organ hypertrophy, altered phenotype and function, and potentially acute organ failure due to fibrosis and loss of contractility.
- MicroRNAs (miRNAs) are increasingly recognized for their role in the pathogenesis of heart failure and bladder dysfunction.
Purpose of the Study:
- To review current knowledge on molecular alterations in the heart and bladder under pressure overload.
- To highlight common signaling pathways and regulatory events involving miRNAs in these organs.
- To explore the therapeutic potential of targeting miRNAs for organ hypertrophy and failure.
Main Methods:
- Literature review of studies on molecular alterations in cardiac and bladder hypertrophy.
- Analysis of miRNA expression patterns and experimental validation of miRNA targets.
- Identification of common signaling pathways in fibrotic remodeling of the heart and bladder.
Main Results:
- Emerging evidence implicates miRNAs in the pathogenesis of heart failure and bladder dysfunction.
- miRNAs regulate gene expression, controlling adaptive and maladaptive organ remodeling processes.
- miRNA expression analysis in the heart provides insights for bladder and other organ research.
- Aberrantly expressed miRNAs present opportunities for pharmacological intervention.
Conclusions:
- miRNAs are crucial in the molecular mechanisms underlying cardiac and bladder hypertrophy and failure.
- Shared signaling pathways and regulatory events exist between the heart and bladder in response to pressure overload.
- Targeting miRNAs offers a promising therapeutic strategy for treating cardiac and bladder diseases characterized by hypertrophy and fibrosis.
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.
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