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Silencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction

dc.contributor.authorEkmekci, Sema Sirma
dc.contributor.authorAKÇAKAYA, Handan
dc.contributor.authorEMRENCE, Zeliha
dc.contributor.authorABACI, Neslihan
dc.contributor.authorSevgiler, Yusuf
dc.contributor.authorTaskin, Eylem
dc.contributor.authorGuven, Celal
dc.contributor.authorKaya, Salih Tunc
dc.contributor.authorSariman, Melda
dc.date.accessioned2021-03-04T19:09:24Z
dc.date.available2021-03-04T19:09:24Z
dc.date.issued2020
dc.identifier.citationTaskin E., Guven C., Kaya S. T. , Sariman M., EMRENCE Z., Ekmekci S. S. , ABACI N., Sevgiler Y., AKÇAKAYA H., "Silencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction", JOURNAL OF BUON, cilt.25, ss.554-565, 2020
dc.identifier.issn1107-0625
dc.identifier.othervv_1032021
dc.identifier.otherav_8e615d5f-fcf3-42b9-ae19-11e1f84c9411
dc.identifier.urihttp://hdl.handle.net/20.500.12627/96199
dc.description.abstractPurpose: Adriamycin (APR) is a commonly used anti-cancer drug. ADR has toxic effects on cardiomyocytes and leads to heart failure. However, the underlying mechanism(s) by which ADR causes heart failure is still not clarified exactly. The aim of present study is to investigate whether ADR-induced heart failure is mediated via HMGB1/TLR4 to initiate the apoptosis through MAPK/AMPK pathways.
dc.language.isoeng
dc.subjectOnkoloji
dc.subjectSağlık Bilimleri
dc.subjectİç Hastalıkları
dc.subjectDahili Tıp Bilimleri
dc.subjectTıp
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectONKOLOJİ
dc.titleSilencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction
dc.typeMakale
dc.relation.journalJOURNAL OF BUON
dc.contributor.departmentOmer Halis Demir University , ,
dc.identifier.volume25
dc.identifier.issue1
dc.identifier.startpage554
dc.identifier.endpage565
dc.contributor.firstauthorID2260082


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