The University of Osaka · 医学
Hikoso教授の研究室では、心不全の発症機構に深く関与する心筋細胞死のメカニズムを解明することを目的としています。特に、NF-κBシグナル経路が圧力負荷に応じて心筋細胞に与える影響を、マウスモデルを用いてin vivoで解析しています。また、STAT6の心筋保護作用についても、血流力学的ストレスに対する耐性機構としての役割を研究しています。
Figures are computed from collected data and may differ slightly.
Cardiomyocyte death plays an important role in the pathogenesis of heart failure. The nuclear factor (NF)-kappaB signaling pathway regulates cell death, however, the effect of NF-kappaB pathway on cell death can vary in different cells or stimuli. The purpose of the present study was to clarify the in vivo role of the NF-kappaB pathway in response to pressure overload. First, we subjected C57Bl6/J mice to pressure overload by means of transverse aortic constriction (TAC) and examined the activit
The protocol was approved by the Institutional Review Board (IRB) of Osaka University Hospital on 24 February 2016 (ID: 15471), and by the IRBs of the all participating facilities. The findings will be disseminated through peer-reviewed publications and conference presentations.
STAT6 plays a protective role against hemodynamic stress in hearts.
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