Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy

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Fältnamn	Indikatorer	Metadata
000		04368naa a2200745 4500
001		oai:openarchive.ki.se:10616/48166
003		SwePub
008		240410s2021 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:gup.ub.gu.se/310644
009		oai:prod.swepub.kib.ki.se:148482339
022		a 2041-1723
024	7	a 10616/481662 hdl
024	7	a http://hdl.handle.net/10616/481662 URI
024	7	a https://doi.org/10.1038/s41467-021-25439-02 DOI
024	7	a https://gup.ub.gu.se/publication/3106442 URI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1484823392 URI
040		a (SwePub)kid (SwePub)gu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Beverborg, Niels Grote4 aut
245	1 0	a Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy
264		c 2021-08-30
264	1	a Stockholm :b Karolinska Institutet, Dept of Cell and Molecular Biology,c 2021
338		a electronic2 rdacarrier
520		a Heart failure (HF) is a major cause of morbidity and mortality worldwide, highlighting an urgent need for novel treatment options, despite recent improvements. Aberrant Ca2+ handling is a key feature of HF pathophysiology. Restoring the Ca2+ regulating machinery is an attractive therapeutic strategy supported by genetic and pharmacological proof of concept studies. Here, we study antisense oligonucleotides (ASOs) as a therapeutic modality, interfering with the PLN/SERCA2a interaction by targeting Pln mRNA for downregulation in the heart of murine HF models. Mice harboring the PLN R14del pathogenic variant recapitulate the human dilated cardiomyopathy (DCM) phenotype; subcutaneous administration of PLN-ASO prevents PLN protein aggregation, cardiac dysfunction, and leads to a 3-fold increase in survival rate. In another genetic DCM mouse model, unrelated to PLN (Cspr3/Mlp−/−), PLN-ASO also reverses the HF phenotype. Finally, in rats with myocardial infarction, PLN-ASO treatment prevents progression of left ventricular dilatation and improves left ventricular contractility. Thus, our data establish that antisense inhibition of PLN is an effective strategy in preclinical models of genetic cardiomyopathy as well as ischemia driven HF.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kardiologi0 (SwePub)302062 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cardiac and Cardiovascular Systems0 (SwePub)302062 hsv//eng
700	1	a Spater, Daniela4 aut
700	1	a Knoll, Ralphu Karolinska Institutet4 aut
700	1	a Hidalgo, Alejandro4 aut
700	1	a Yeh, Steve T4 aut
700	1	a Elbeck, Zaher4 aut
700	1	a Sillje, Herman H W4 aut
700	1	a Eijgenraam, Tim R4 aut
700	1	a Siga, Humam4 aut
700	1	a Zurek, Magdalena4 aut
700	1	a Palmér, Malinu Gothenburg University,Göteborgs universitet,Core Facilities, Experimentell Biomedicin,Core Facilities, Experimental Biomedicine4 aut0 (Swepub:gu)xpamal
700	1	a Pehrsson, Susanne4 aut
700	1	a Albery, Tamsin4 aut
700	1	a Bomer, Nils4 aut
700	1	a Hoes, Martijn F4 aut
700	1	a Boogerd, Cornelis J4 aut
700	1	a Frisk, Michael4 aut
700	1	a van Rooij, Eva4 aut
700	1	a Damle, Sagar4 aut
700	1	a Louch, William E4 aut
700	1	a Wang, Qing-Dong4 aut
700	1	a Fritsche-Danielson, Regina4 aut
700	1	a Chien, Kenneth R4 aut
700	1	a Hansson, Kenny M4 aut
700	1	a Mullick, Adam E4 aut
700	1	a de Boer, Rudolf A4 aut
700	1	a van der Meer, Peter4 aut
710	2	a Karolinska Institutetb Core Facilities, Experimentell Biomedicin4 org
710	2	a Karolinska Institutet
710	2	a Karolinska Institutet
773	0	t Nature Communicationsd Stockholm : Karolinska Institutet, Dept of Cell and Molecular Biologyx 2041-1723
856	4	u http://hdl.handle.net/10616/48166x primaryx Object in contextx freey FULLTEXT
856	4	u https://www.nature.com/articles/s41467-021-25439-0.pdf
856	4 8	u http://hdl.handle.net/10616/48166
856	4 8	u https://doi.org/10.1038/s41467-021-25439-0
856	4 8	u https://gup.ub.gu.se/publication/310644
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:148482339

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