Molecular switches under TGFβ signalling during progression from cardiac hypertrophy to heart failure

Cardiac hypertrophy is a mechanism to compensate for increased cardiac work load, that is, after myocardial infarction or upon pressure overload. However, in the long run cardiac hypertrophy is a prevailing risk factor for the development of heart failure. During pathological remodelling processes l...

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Bibliographic Details
Published inBritish journal of pharmacology Vol. 173; no. 1; pp. 3 - 14
Main Authors Heger, J, Schulz, R, Euler, G
Format Journal Article
LanguageEnglish
Published England John Wiley and Sons Inc 01.01.2016
Subjects
Animals
Apoptosis
Cardiomegaly - metabolism
Cardiomegaly - pathology
Disease Progression
Energy Metabolism
Fibrosis - metabolism
Fibrosis - pathology
Heart Failure - metabolism
Heart Failure - pathology
Humans
MAP Kinase Kinase Kinases - metabolism
MicroRNAs - metabolism
Mitochondria - metabolism
Models, Biological
Myocytes, Cardiac - pathology
Receptors, Adrenergic, beta - metabolism
Review
Signal Transduction
Transforming Growth Factor beta - metabolism
Ubiquitin - metabolism
Ventricular Remodeling
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Summary:Cardiac hypertrophy is a mechanism to compensate for increased cardiac work load, that is, after myocardial infarction or upon pressure overload. However, in the long run cardiac hypertrophy is a prevailing risk factor for the development of heart failure. During pathological remodelling processes leading to heart failure, decompensated hypertrophy, death of cardiomyocytes by apoptosis or necroptosis and fibrosis as well as a progressive dysfunction of cardiomyocytes are apparent. Interestingly, the induction of hypertrophy, cell death or fibrosis is mediated by similar signalling pathways. Therefore, tiny changes in the signalling cascade are able to switch physiological cardiac remodelling to the development of heart failure. In the present review, we will describe examples of these molecular switches that change compensated hypertrophy to the development of heart failure and will focus on the importance of the signalling cascades of the TGFβ superfamily in this process. In this context, potential therapeutic targets for pharmacological interventions that could attenuate the progression of heart failure will be discussed.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ObjectType-Review-1
ISSN:0007-1188
1476-5381
DOI:10.1111/bph.13344