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2017 Fiscal Year Final Research Report

Endothelial dysfunction after lung transplantation with donation after cardiac death donors

Research Project

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Project/Area Number 26462128
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Respiratory surgery
Research InstitutionEhime University

Principal Investigator

Okazaki Mikio  愛媛大学, 医学部附属病院, 助教 (50467750)

Co-Investigator(Kenkyū-buntansha) 佐野 由文  愛媛大学, 医学系研究科, 准教授 (60322228)
Project Period (FY) 2014-04-01 – 2018-03-31
Keywords肺移植 / 虚血再灌流障害 / 心停止ドナー
Outline of Final Research Achievements

The purpose of this study was to elucidate molecular mechanism of ischemia reperfusion injury after lung transplantation with donation after cardiac death donors and to reduce lung transplantation with donation after cardiac death donors by using mouse model. Endothelial cells of donor lung were destroyed during ischemia period, and the inhibition of endothelial dysfunction is thought to be important on the reduction of ischemia reperfusion injury. R-spondin 3 which has been reported to tighten of endothelial cell junctions reduced lung warm ischemia reperfusion injury. Tightening of endothelial cell junctions was considered to contribute on the inhibition of lung warm ischemia reperfusion injury.

Free Research Field

肺移植

URL: 

Published: 2019-03-29  

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