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Syndecan-4 is a key determinant of collagen cross-linking and passive myocardial stiffness in the pressure-overloaded heart
Author(s) -
Kate M. Herum,
Ida G. Lunde,
Biljana Skrbic,
William E. Louch,
Almira Hasic,
Sigurd Boye,
Andreas Unger,
Sverre-Henning Brorson,
Ivar Sjaastad,
Theis Tønnessen,
Wolfgang A. Linke,
Maria F. Gomez,
Geir Christensen
Publication year - 2015
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvv002
Subject(s) - syndecan 1 , pressure overload , nfat , myofibroblast , lysyl oxidase , extracellular matrix , microbiology and biotechnology , medicine , endocrinology , osteopontin , cardiac fibrosis , myocyte , chemistry , biology , muscle hypertrophy , fibrosis , calcineurin , biochemistry , cell , transplantation , cardiac hypertrophy
Diastolic dysfunction is central to the development of heart failure. To date, there is no effective treatment and only limited understanding of its molecular basis. Recently, we showed that the transmembrane proteoglycan syndecan-4 increases in the left ventricle after pressure overload in mice and man, and that syndecan-4 via calcineurin/nuclear factor of activated T-cells (NFAT) promotes myofibroblast differentiation and collagen production upon mechanical stress. The aim of this study was to investigate whether syndecan-4 affects collagen cross-linking and myocardial stiffening in the pressure-overloaded heart.

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