Syndecan-4 is a key determinant of collagen cross-linking and passive myocardial stiffness in the pressure-overloaded heart.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Abstract

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.

Detaljer

Författare
  • Kate Herum Möller
  • 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 Gomez
  • Geir Christensen
Enheter & grupper
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Kardiologi
Originalspråkengelska
Sidor (från-till)217-226
TidskriftCardiovascular Research
Volym106
Utgivningsnummer2
StatusPublished - 2015
PublikationskategoriForskning
Peer review utfördJa