ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling af...
ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure overload
About this item
Full title
Author / Creator
Rypdal, Karoline B. , Olav Melleby, A. , Robinson, Emma L. , Li, Jia , Palmero, Sheryl , Seifert, Deborah E. , Martin, Daniel , Clark, Catelyn , López, Begoña , Andreassen, Kristine , Dahl, Christen P. , Sjaastad, Ivar , Tønnessen, Theis , Stokke, Mathis K. , Louch, William E. , González, Arantxa , Heymans, Stephane , Christensen, Geir , Apte, Suneel S. and Lunde, Ida G.
Publisher
London: Nature Publishing Group UK
Journal title
Language
English
Formats
Publication information
Publisher
London: Nature Publishing Group UK
Subjects
More information
Scope and Contents
Contents
Heart failure is a major cause of morbidity and mortality worldwide, and can result from pressure overload, where cardiac remodelling is characterized by cardiomyocyte hypertrophy and death, fibrosis, and inflammation. In failing hearts, transforming growth factor (TGF)β drives cardiac fibroblast (CFB) to myofibroblast differentiation causing exces...
Alternative Titles
Full title
ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure overload
Authors, Artists and Contributors
Author / Creator
Olav Melleby, A.
Robinson, Emma L.
Li, Jia
Palmero, Sheryl
Seifert, Deborah E.
Martin, Daniel
Clark, Catelyn
López, Begoña
Andreassen, Kristine
Dahl, Christen P.
Sjaastad, Ivar
Tønnessen, Theis
Stokke, Mathis K.
Louch, William E.
González, Arantxa
Heymans, Stephane
Christensen, Geir
Apte, Suneel S.
Lunde, Ida G.
Identifiers
Primary Identifiers
Record Identifier
TN_cdi_doaj_primary_oai_doaj_org_article_8dc2cdb39a0043879864fac9c8cf91a5
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_8dc2cdb39a0043879864fac9c8cf91a5
Other Identifiers
ISSN
2399-3642
E-ISSN
2399-3642
DOI
10.1038/s42003-022-04361-1
