Exploration for novel therapeutic target of inflammation and heart failure induced by accumulation of mtDNA

2015 Fiscal Year Final Research Report

• Project/Area Number: 25713031
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Osaka University
• Principal Investigator: Oka Takafumi 大阪大学, 医学(系)研究科(研究院), 特任研究員 (30647285)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: ミトコンドリア / 炎症 / 心不全

Outline of Final Research Achievements

We have previously reported that the accumulation of mitochondrial DNA in cardiomyocytes can induce inflammatory response and heart failure. Mitochondria are usually degraded through mitochondria-specific autophagy, mitophagy. In yeast, Atg32 was found to be an essential molecule during mitophagy, however, no functional homologue for Atg32 in mammalian cells had been identified. In this research we investigated a novel molecular mechanism involved in the mitophagy in mammalian cells, and found BCL2L13 as a functional homologue of Atg32. BCL2L13 induced mitochondrial fragmentation and played an important role as a mitophagic receptor on outer mitochondrial membrane.

Free Research Field

循環器内科学