Show simple item record

dc.contributor.authorSzabó, Zoltán
dc.contributor.authorVainio, Laura
dc.contributor.authorLin, Ruizhu
dc.contributor.authorSwan, Julia
dc.contributor.authorHulmi, Juha J.
dc.contributor.authorRahtu-Korpela, Lea
dc.contributor.authorSerpi, Raisa
dc.contributor.authorLaitinen, Mika
dc.contributor.authorPasternack, Arja
dc.contributor.authorRitvos, Olli
dc.contributor.authorKerkelä, Risto
dc.contributor.authorMagga, Johanna
dc.date.accessioned2020-06-02T03:55:23Z
dc.date.available2020-06-02T03:55:23Z
dc.date.issued2020
dc.identifier.citationSzabó, Z., Vainio, L., Lin, R., Swan, J., Hulmi, J. J., Rahtu-Korpela, L., Serpi, R., Laitinen, M., Pasternack, A., Ritvos, O., Kerkelä, R., & Magga, J. (2020). Systemic Blockade of ACVR2B Ligands Attenuates Muscle Wasting in Ischemic Heart Failure Without Compromising Cardiac Function. <i>FASEB Journal</i>, <i>34</i>(8), 9911-9924. <a href="https://doi.org/10.1096/fj.201903074RR" target="_blank">https://doi.org/10.1096/fj.201903074RR</a>
dc.identifier.otherCONVID_35831322
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/69359
dc.description.abstractSignaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blockade of ACVR2B ligands did not rescue the heart from ischemic injury or alleviate post-MI remodeling and ischemic HF. Collectively, ACVR2B-Fc did not affect cardiomyocyte hypertrophy, fibrosis, angiogenesis, nor factors associated with cardiac regeneration except modification of certain genes involved in metabolism or cell growth/survival. ACVR2B-Fc, however, was able to reduce skeletal muscle wasting in chronic ischemic HF, accompanied by reduced LC3II as a marker of autophagy and increased mTOR signaling and Cited4 expression as markers of physiological hypertrophy in quadriceps muscle. Our results ascertain pharmacological blockade of ACVR2B ligands as a possible therapy for skeletal muscle wasting in ischemic HF. Pharmacological blockade of ACVR2B ligands preserved myofiber size in ischemic HF, but did not compromise cardiac function nor exacerbate cardiac remodeling after ischemic injury.en
dc.format.mimetypeapplication/pdf
dc.languageeng
dc.language.isoeng
dc.publisherJohn Wiley & Sons; Federation of American Societies for Experimental Biology
dc.relation.ispartofseriesFASEB Journal
dc.rightsCC BY-NC 4.0
dc.subject.otheractivins
dc.subject.othergrowth differentiation factors
dc.subject.othermyocardial infarction
dc.titleSystemic Blockade of ACVR2B Ligands Attenuates Muscle Wasting in Ischemic Heart Failure Without Compromising Cardiac Function
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-202006023617
dc.contributor.laitosLiikuntatieteellinen tiedekuntafi
dc.contributor.laitosFaculty of Sport and Health Sciencesen
dc.contributor.oppiaineLiikuntafysiologiafi
dc.contributor.oppiaineExercise Physiologyen
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.description.reviewstatuspeerReviewed
dc.format.pagerange9911-9924
dc.relation.issn0892-6638
dc.relation.numberinseries8
dc.relation.volume34
dc.type.versionpublishedVersion
dc.rights.copyright© 2020 The Authors
dc.rights.accesslevelopenAccessfi
dc.relation.grantnumber275922
dc.subject.ysosoluviestintä
dc.subject.ysosydäninfarkti
dc.subject.ysosydänlihassolut
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p28740
jyx.subject.urihttp://www.yso.fi/onto/yso/p8730
jyx.subject.urihttp://www.yso.fi/onto/yso/p38718
dc.rights.urlhttps://creativecommons.org/licenses/by-nc/4.0/
dc.relation.doi10.1096/fj.201903074RR
dc.relation.funderSuomen Akatemiafi
dc.relation.funderAcademy of Finlanden
jyx.fundingprogramAkatemiatutkijan tehtävä, SAfi
jyx.fundingprogramResearch post as Academy Research Fellow, AoFen
jyx.fundinginformationAcademy of Finland (Suomen Akatemia). Grant Numbers: 268505, 297094, 275922 Sydäntutkimussäätiö (Finnish Foundation for Cardiovascular Research)


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

CC BY-NC 4.0
Except where otherwise noted, this item's license is described as CC BY-NC 4.0