Communications Biology (Dec 2022)

ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure overload

  • Karoline B. Rypdal,
  • A. Olav Melleby,
  • Emma L. Robinson,
  • Jia Li,
  • Sheryl Palmero,
  • Deborah E. Seifert,
  • Daniel Martin,
  • Catelyn Clark,
  • Begoña López,
  • Kristine Andreassen,
  • Christen P. Dahl,
  • Ivar Sjaastad,
  • Theis Tønnessen,
  • Mathis K. Stokke,
  • William E. Louch,
  • Arantxa González,
  • Stephane Heymans,
  • Geir Christensen,
  • Suneel S. Apte,
  • Ida G. Lunde

DOI
https://doi.org/10.1038/s42003-022-04361-1
Journal volume & issue
Vol. 5, no. 1
pp. 1 – 15

Abstract

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The role of ADAMTSL3 in heart pathology and cardiac disease is investigated with Adamtsl3-deficient mice using CRISPR-Cas9 gene editing.