Unraveling the mechanism by which G0S2 regulates mitochondrial ATP production under ischemia

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19378
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Osaka University
• Principal Investigator: Kato Hisakazu 大阪大学, 医学系研究科, 助教 (30589312)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: ミトコンドリア / 虚血 / ATP合成酵素 / タンパク質分解

Outline of Final Research Achievements

Heart tissue consumes more energy than other organs to maintain cardiac pump function. However, the mechanism by which mitochondrial ATP production is regulated under hypoxia is not fully understood. In this study, we revealed how G0S2 regulates mitochondrial ATP production via ATP synthase, mainly from the following experiments. (1) G0S2 is degraded by ubiquitin-proteasome system. (2) One amino acid within hydrophobic region of G0S2 is strongly involved in its protein degradation. (3) In cardiomyocytes, G0S2 mutants that have longer half-life improved the decreases in mitochondrial ATP concentration under hypoxic condition compared to wild-type. These results suggest that the enhancement of mitochondrial ATP production by inhibition of G0S2 protein degradation can lead to novel therapeutic target to ischemic heart diseases.

Free Research Field

分子心臓学