Elucidation of molecualr mechanism underlying cardiac hibernation by reactive persulfide species

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K14959
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Biological pharmacy
• Research Institution: Okazaki Research Facilities, National Institutes of Natural Sciences
• Principal Investigator: Motohiro Nishida 大学共同利用機関法人自然科学研究機構(岡崎共通研究施設), 岡崎統合バイオサイエンスセンター, 教授 (90342641)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 循環器 / 薬理学 / 生理学 / レドックス / 親電子 / イオウ

Outline of Final Research Achievements

We utilize oxygen as a source to generate energy. In contrast, oxygen easily converts to more electrophilic substrate (electophile) and electrophile irreversibly modifies intracellular molecules, resulting in the development of diseases. We revealed that intracellular nucleophilic sulfur species (reactive persulfide species) act as chelator of electrophile to eliminate electrophilic modifications in cells. We also identified a key enzyme generating reactive persulfide species, and overexpression of this enzyme in cardiac cells was found to reduce the risk of heart failure in mice.

Free Research Field

薬理学