Cardiomyocyte-derived fibrosis as driver of cardiomyopathy: invited editorial

This editorial refers to ‘Cardiomyocyte SORBS2 expression increases in heart failure and regulates integrin interactions and extracellular matrix composition’, by L.T. Timmer et al., https://doi.org/10.1093/cvr/cvaf021.Cardiac fibrosis describes pathological deposition of extracellular matrix (ECM),...

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Main Authors: Martin Garrido, Abel (Author) , Heineke, Jörg (Author)
Format: Article (Journal) Editorial
Language:English
Published: March 2025
In: Cardiovascular research
Year: 2025, Volume: 121, Issue: 4, Pages: 528-529
ISSN:1755-3245
DOI:10.1093/cvr/cvaf025
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.1093/cvr/cvaf025
Verlag, kostenfrei, Volltext: https://academic.oup.com/cardiovascres/article/121/4/528/8045731
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Author Notes:Abel Martin-Garrido and Joerg Heineke

MARC

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520 |a This editorial refers to ‘Cardiomyocyte SORBS2 expression increases in heart failure and regulates integrin interactions and extracellular matrix composition’, by L.T. Timmer et al., https://doi.org/10.1093/cvr/cvaf021.Cardiac fibrosis describes pathological deposition of extracellular matrix (ECM), which can either be the consequence of cardiomyocyte death in ‘replacement fibrosis’ or emerge as ‘reactive fibrosis’ during mechanical or metabolic overload in the absence of significant cardiomyocyte death. Excessive fibrosis and its chronification inevitably lead the progression of heart failure, mainly due to stiffening of the myocardium and predisposition to lethal arrhythmia. To identify new therapeutic strategies, underlying mechanisms and cell types need to be deciphered by basic research. 
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